Acute Inflammation and Its Mediators
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Questions and Answers

Which of the following statements correctly describes the function of C3b in the complement system?

  • C3b is a chemotactic factor for neutrophils.
  • C3b serves as an opsonin for phagocytosis. (correct)
  • C3b triggers mast cell degranulation.
  • C3b forms part of the membrane attack complex (MAC).

    • What is the role of bradykinin in the inflammatory response?

  • It activates the complement system directly.
  • It induces histamine release from mast cells.
  • It forms the membrane attack complex.
  • It mediates vasodilation and increases vascular permeability. (correct)

    • Which pathway of complement activation directly involves microbial products?

  • Alternative pathway (correct)
  • Classical pathway
  • Coagulation pathway
  • Mannose-binding lectin pathway

    • Which mediator is primarily responsible for the vasodilation associated with the immediate response in inflammation?

    <p>Histamine</p> Signup and view all the answers

    How does the activation of Hageman factor (Factor XII) contribute to inflammation?

    <p>It activates the coagulation and fibrinolytic systems.</p> Signup and view all the answers

    What is the primary effect of C5a in the context of inflammation?

    <p>It serves as a chemotactic factor for neutrophils.</p> Signup and view all the answers

    The release of arachidonic acid metabolites after tissue injury leads to which response?

    <p>Delayed immune response.</p> Signup and view all the answers

    The production of C3 convertase is crucial for which of the following processes in the complement system?

    <p>Cleaving C3 into C3a and C3b.</p> Signup and view all the answers

    What cellular response characterizes acute inflammation?

    <p>Presence of edema and neutrophils in tissue</p> Signup and view all the answers

    Which mediator is activated by pathogen-associated molecular patterns (PAMPs)?

    <p>Toll-like receptors (TLRs)</p> Signup and view all the answers

    What is the main role of cyclooxygenase in inflammation?

    <p>Production of prostaglandins that mediate vasodilation</p> Signup and view all the answers

    Which type of inflammation is characterized by both neutrophils' presence and a response to tissue necrosis?

    <p>Acute inflammation</p> Signup and view all the answers

    What is the function of LTB4 in the context of acute inflammation?

    <p>Attracts and activates neutrophils</p> Signup and view all the answers

    What role do mast cells play in the inflammatory process?

    <p>Release histamine and other mediators</p> Signup and view all the answers

    How does NF-κB contribute to the inflammatory response?

    <p>Activating immune response genes</p> Signup and view all the answers

    What is the primary result of TLR activation in the immune system?

    <p>Upregulation of immune response genes</p> Signup and view all the answers

    What role does histamine play in vascular response during inflammation?

    <p>It increases vascular permeability by causing endothelial cell contraction.</p> Signup and view all the answers

    Which of the following is a key mediator that sensitizes sensory nerve endings?

    <p>Bradykinin</p> Signup and view all the answers

    What is the primary effect of fluid leakage from postcapillary venules during inflammation?

    <p>It causes the accumulation of exudate in the interstitial space.</p> Signup and view all the answers

    What impact does tissue damage have on endothelial cells during inflammation?

    <p>It results in endothelial cell disruption.</p> Signup and view all the answers

    During inflammation, which mediator is specifically mentioned as causing pain?

    <p>Prostaglandin E2 (PGE2)</p> Signup and view all the answers

    Which process primarily increases permeability in postcapillary venules during inflammation?

    <p>Endothelial cell disruption</p> Signup and view all the answers

    What type of fluid is released into the interstitial space due to leakage from postcapillary venules?

    <p>Exudate</p> Signup and view all the answers

    Which of the following statements about bradykinin is true?

    <p>It sensitizes pain receptors to induce pain sensation.</p> Signup and view all the answers

    Exudate is fluid that leaks from postcapillary venules into the interstitial space.

    <p>True</p> Signup and view all the answers

    Histamine causes endothelial cell disruption during inflammation.

    <p>False</p> Signup and view all the answers

    Bradykinin and PGE2 progressively desensitize sensory nerve endings.

    <p>False</p> Signup and view all the answers

    Endothelial cell contraction is one of the effects triggered by bradykinin.

    <p>False</p> Signup and view all the answers

    Tissue damage during inflammation leads to the release of mediators that sensitize pain receptors.

    <p>True</p> Signup and view all the answers

    The presence of pain (dolor) is only due to bradykinin in the inflammatory response.

    <p>False</p> Signup and view all the answers

    A key mediator of the inflammatory response causes endothelial cells to contract.

    <p>True</p> Signup and view all the answers

    The fluid released from postcapillary venules during inflammation is referred to as transudate.

    <p>False</p> Signup and view all the answers

    Acute inflammation is characterized primarily by the absence of edema in tissue.

    <p>False</p> Signup and view all the answers

    Arachidonic acid is released from the cell membrane by phospholipase A2 during acute inflammation.

    <p>True</p> Signup and view all the answers

    Toll-like receptors (TLRs) are found solely on cells of the innate immune system.

    <p>False</p> Signup and view all the answers

    Lipopolysaccharides are recognized by CD14, a co-receptor for TLR4, during innate immunity.

    <p>True</p> Signup and view all the answers

    The activation of NF-κB leads to the downregulation of immune response genes.

    <p>False</p> Signup and view all the answers

    PGE2 only influences vascular permeability but has no effect on pain or fever.

    <p>False</p> Signup and view all the answers

    Mast cells play a critical role in the release of arachidonic acid metabolites.

    <p>False</p> Signup and view all the answers

    Leukotrienes produced by 5-lipoxygenase specifically mediate vasodilation.

    <p>False</p> Signup and view all the answers

    C5b forms the membrane attack complex (MAC) by complexing with C6, C7, C8, and C9.

    <p>True</p> Signup and view all the answers

    Hageman factor (Factor XII) is activated by exposure to endothelial cells.

    <p>False</p> Signup and view all the answers

    Leukotrienes are primarily involved in the immediate response of inflammation.

    <p>False</p> Signup and view all the answers

    C3a and C5a function as anaphylatoxins that mediate vasodilation and increased vascular permeability.

    <p>True</p> Signup and view all the answers

    The kinin system produces bradykinin, which has no effect on vascular permeability.

    <p>False</p> Signup and view all the answers

    The classical pathway of complement activation is initiated by C1 binding to antigen-bound IgE.

    <p>False</p> Signup and view all the answers

    Increased blood flow leading to redness and warmth during inflammation is primarily due to bradykinin.

    <p>False</p> Signup and view all the answers

    C3b acts as an opsonin, facilitating phagocytosis of microbes.

    <p>True</p> Signup and view all the answers

    What role do histamine and tissue damage play in the function of endothelial cells during inflammation?

    <p>Histamine causes endothelial cell contraction, while tissue damage leads to endothelial cell disruption.</p> Signup and view all the answers

    Explain how bradykinin and PGE2 are involved in pain perception during inflammation.

    <p>Bradykinin and PGE2 sensitize sensory nerve endings, enhancing the perception of pain at the injury site.</p> Signup and view all the answers

    Describe the type of fluid that results from the leakage of postcapillary venules during inflammation.

    <p>The fluid leaking from postcapillary venules is referred to as exudate.</p> Signup and view all the answers

    What is the significance of increased permeability in postcapillary venules during the inflammatory response?

    <p>Increased permeability allows the escape of immune cells and proteins to the site of injury to facilitate healing.</p> Signup and view all the answers

    How does tissue damage affect the release of inflammatory mediators?

    <p>Tissue damage triggers the release of mediators, such as histamine and bradykinin, which exacerbate inflammation.</p> Signup and view all the answers

    What is the relationship between endothelial cell contraction and the inflammatory process?

    <p>Endothelial cell contraction increases the permeability of blood vessels, allowing inflammatory cells to exit the bloodstream.</p> Signup and view all the answers

    How do bradykinin and histamine collectively influence vascular responses during inflammation?

    <p>Bradykinin and histamine together cause vasodilation and increased vascular permeability, enhancing blood flow to the affected area.</p> Signup and view all the answers

    What impact does the activation of endothelial cells have during the inflammatory response?

    <p>Activated endothelial cells express adhesion molecules that facilitate the recruitment of leukocytes to the site of inflammation.</p> Signup and view all the answers

    What triggers the immediate response in inflammation, particularly in terms of mediator release?

    <p>The immediate response is triggered by tissue trauma, complement proteins C3a and C5a, or cross-linking of cell-surface IgE by antigen.</p> Signup and view all the answers

    Explain the role of C3 convertase in the complement system.

    <p>C3 convertase mediates the conversion of C3 to C3a and C3b, crucial for activating the complement cascade.</p> Signup and view all the answers

    How does C5a contribute to inflammation beyond vasodilation?

    <p>C5a is chemotactic for neutrophils, guiding them to sites of inflammation to participate in the immune response.</p> Signup and view all the answers

    What is the function of bradykinin in the context of inflammation?

    <p>Bradykinin mediates vasodilation and increases vascular permeability, contributing to the inflammatory response.</p> Signup and view all the answers

    Describe the final outcome of the complement system's activation.

    <p>The final outcome involves the formation of the membrane attack complex (MAC), which lyses microbes by creating pores in their membranes.</p> Signup and view all the answers

    What mechanisms does the kinin system activate upon its initiation?

    <p>The kinin system is activated to produce bradykinin, which mediates vasodilation and increases vascular permeability, similar to histamine.</p> Signup and view all the answers

    What is the significance of the classical and alternative pathways in the complement activation process?

    <p>The classical pathway is initiated by antibody-antigen complexes, while the alternative pathway activates through microbial products, both leading to C3 convertase formation.</p> Signup and view all the answers

    How do activated mast cells influence the inflammatory process?

    <p>Activated mast cells release histamine and other mediators that enhance vasodilation and vascular permeability during inflammation.</p> Signup and view all the answers

    What role do Toll-like receptors (TLRs) play in the context of acute inflammation?

    <p>TLRs activate signaling pathways in response to pathogen-associated molecular patterns (PAMPs), leading to the production of multiple immune mediators and the activation of immune response genes.</p> Signup and view all the answers

    Explain how arachidonic acid metabolites contribute to inflammation.

    <p>Arachidonic acid metabolites, such as prostaglandins and leukotrienes, mediate various inflammatory responses including vasodilation, increased vascular permeability, and pain.</p> Signup and view all the answers

    Describe the immediate physiological changes associated with acute inflammation.

    <p>Acute inflammation is characterized by edema, increased vascular permeability, and recruitment of neutrophils to the affected tissue.</p> Signup and view all the answers

    What is the significance of NF-κB activation in inflammatory responses?

    <p>NF-κB activation leads to the transcription of genes responsible for producing multiple immune response mediators, essential for mounting an effective response.</p> Signup and view all the answers

    Outline the primary function of mast cells in the inflammatory process.

    <p>Mast cells release various mediators, including histamines and arachidonic acid metabolites, which play roles in vasodilation and promoting inflammation.</p> Signup and view all the answers

    How do leukotrienes produced by 5-lipoxygenase affect the inflammatory response?

    <p>Leukotrienes such as LTB4 attract and activate neutrophils, while others mediate vasoconstriction and increased vascular permeability.</p> Signup and view all the answers

    What are the two classifications of inflammation, and how do they differ?

    <p>Inflammation is classified as acute, characterized by rapid onset and neutrophilic response, and chronic, which involves prolonged inflammation and may include different immune cells like lymphocytes.</p> Signup and view all the answers

    Discuss the role of PAMPs in the activation of the innate immune system.

    <p>PAMPs are molecular patterns found on pathogens that are recognized by TLRs, leading to the activation of immune responses aimed at eliminating infections.</p> Signup and view all the answers

    Due to leakage of fluid from postcapillary venules into the interstitial space, this type of fluid is referred to as ______.

    <p>exudate</p> Signup and view all the answers

    One of the key mediators that causes endothelial cell contraction is ______.

    <p>histamine</p> Signup and view all the answers

    Bradykinin and PGE2 sensitizes sensory nerve endings, contributing to the sensation of ______.

    <p>pain</p> Signup and view all the answers

    The presence of pain in the context of inflammation is referred to as ______.

    <p>dolor</p> Signup and view all the answers

    Disruption of endothelial cells can result from ______ during inflammation.

    <p>tissue damage</p> Signup and view all the answers

    Increased permeability in postcapillary venules during inflammation is primarily due to the action of ______.

    <p>histamine</p> Signup and view all the answers

    Bradykinin is specifically mentioned as a mediator that causes ______ in the inflammatory response.

    <p>pain</p> Signup and view all the answers

    Fluid leakage from postcapillary venules results in the accumulation of ______ in the interstitial space.

    <p>exudate</p> Signup and view all the answers

    Acute inflammation is characterized by the presence of edema and ______ in tissue.

    <p>neutrophils</p> Signup and view all the answers

    Toll-like receptors (TLRs) are activated by pathogen-associated molecular ______ (PAMPs).

    <p>patterns</p> Signup and view all the answers

    Cyclooxygenase produces ______ which mediate vasodilation and increase vascular permeability.

    <p>prostaglandins</p> Signup and view all the answers

    Arachidonic acid is released from the cell membrane by ______ A2.

    <p>phospholipase</p> Signup and view all the answers

    CD14 on macrophages recognizes lipopolysaccharide, a ______, on the outer membrane of gram-negative bacteria.

    <p>PAMP</p> Signup and view all the answers

    Mast cells are widely distributed throughout ______ tissue.

    <p>connective</p> Signup and view all the answers

    The activation of NF-κB leads to the upregulation of immune response ______ that activate genes.

    <p>genes</p> Signup and view all the answers

    Leukotrienes produced by 5-lipoxygenase mediate ______, bronchospasm, and increased vascular permeability.

    <p>vasoconstriction</p> Signup and view all the answers

    The immediate response to tissue trauma involves release of preformed ______ granules.

    <p>histamine</p> Signup and view all the answers

    C3 convertase mediates the conversion of C3 to ______ and C3b.

    <p>C3a</p> Signup and view all the answers

    The ______ factor (Factor XII) is activated upon exposure to subendothelial collagen.

    <p>Hageman</p> Signup and view all the answers

    C5a is known to be ______ for neutrophils during inflammation.

    <p>chemotactic</p> Signup and view all the answers

    The classical pathway of complement activation is initiated by C1 binding to ______ that is bound to antigen.

    <p>IgG</p> Signup and view all the answers

    The kinin system mediates the production of ______, which causes vasodilation and increased vascular permeability.

    <p>bradykinin</p> Signup and view all the answers

    Leukotrienes are particularly involved in the ______ response following tissue injury.

    <p>delayed</p> Signup and view all the answers

    C3b acts as an ______ in the process of phagocytosis.

    <p>opsonin</p> Signup and view all the answers

    Match the following mediators with their respective effects during inflammation:

    <p>Histamine = Endothelial cell contraction Bradykinin = Sensitization of sensory nerve endings PGE2 = Pain perception enhancement Tissue damage = Endothelial cell disruption</p> Signup and view all the answers

    Match the following processes with their triggers or consequences during inflammation:

    <p>Fluid leakage from postcapillary venules = Exudate formation Endothelial cell contraction = Vasodilation Bradykinin release = Nerve ending sensitization Tissue injury = Release of inflammatory mediators</p> Signup and view all the answers

    Match the following terms with their definitions related to inflammation:

    <p>Exudate = Fluid leaking into interstitial space due to inflammation Vasodilation = Widening of blood vessels leading to increased blood flow Sensitization = Process of increasing pain sensitivity Endothelial disruption = Damage to blood vessel linings due to inflammation</p> Signup and view all the answers

    Match the following inflammatory mediators with their primary roles:

    <p>Histamine = Triggers vascular permeability increase Bradykinin = Stimulates pain response PGE2 = Mediates fever and amplifies pain Tissue damage = Activates inflammatory pathways</p> Signup and view all the answers

    Match the following inflammatory responses with their corresponding mediators:

    <p>Increased vascular permeability = Histamine Sensitized nerve endings = Bradykinin Endothelial disruption = Tissue damage Pain amplification = PGE2</p> Signup and view all the answers

    Match the inflammatory symptoms with their causal mediators:

    <p>Pain (dolor) = Bradykinin and PGE2 Swelling = Exudate formation Redness = Increased blood flow Heat = Vasodilation</p> Signup and view all the answers

    Match the following mechanisms of inflammation with their effects:

    <p>Histamine release = Increases permeability of blood vessels Bradykinin action = Sensitizes pain receptors PGE2 production = Facilitates pain signaling Tissue damage result = Disruption of endothelial cells</p> Signup and view all the answers

    Match the following aspects of inflammation with their outcomes:

    <p>Fluid moving into tissues = Results in swelling (edema) Release of chemical mediators = Initiates pain response Endothelial cell contraction = Increases leukocyte migration Tissue damage = Promotes inflammatory reactions</p> Signup and view all the answers

    Match the following inflammatory mediators with their functions:

    <p>Histamine = Mediates vasodilation of arterioles C3a = Anaphylatoxin that triggers mast cell degranulation Bradykinin = Mediates pain and increases vascular permeability C5a = Chemotactic factor for neutrophils</p> Signup and view all the answers

    Match the pathways of complement activation to their initiating factors:

    <p>Classical pathway = C1 binds to antigen-bound IgG or IgM Alternative pathway = Microbial products directly activate complement MBL pathway = MBL binds to mannose on microorganisms C5 convertase = Mediates C5 to C5a and C5b production</p> Signup and view all the answers

    Match the effects of cytokines or mediators to their characteristics:

    <p>Histamine = Preformed granule release from mast cells Leukotrienes = Produced from arachidonic acid metabolites C3b = Acts as an opsonin for phagocytosis MAC = Lyses microbes by creating a hole in the cell membrane</p> Signup and view all the answers

    Match the components of the kinin system with their roles:

    <p>High-molecular-weight kininogen = Cleaved to produce bradykinin Bradykinin = Mediates vasodilation and increased permeability Hageman factor (Factor XII) = Activates the kinin system upon tissue injury C3a = Involved in vasodilation and mast cell activation</p> Signup and view all the answers

    Match the cardinal signs of inflammation with their causes:

    <p>Redness (rubor) = Increased blood flow from vasodilation Swelling (tumor) = Fluid leakage from postcapillary venules Warmth (calor) = Increased blood flow and metabolic activity Pain (dolor) = Mediated by bradykinin and other substances</p> Signup and view all the answers

    Match the immune system components activated by Hageman factor (Factor XII):

    <p>Coagulation system = Initiates blood clot formation Fibrinolytic system = Breaks down blood clots Complement system = Enhances the inflammatory response Kinin system = Produces mediators that increase permeability and pain</p> Signup and view all the answers

    Match the inflammatory responses with the corresponding processes:

    <p>Immediate response = Release of preformed histamine granules Delayed response = Production of arachidonic acid metabolites Mast cell degranulation = Triggered by C3a and C5a Vasodilation = Mediated by histamine and prostaglandins</p> Signup and view all the answers

    Match the complement components with their specific roles:

    <p>C3a = Increases vascular permeability C3b = Opsonizes pathogens for phagocytosis C5a = Stimulates chemotaxis of neutrophils C5b = Initiates formation of the membrane attack complex</p> Signup and view all the answers

    Match the following mediators of acute inflammation with their functions:

    <p>Prostaglandins = Mediate vasodilation and increased vascular permeability Leukotrienes = Attract and activate neutrophils Toll-like receptors = Recognize pathogen-associated molecular patterns Arachidonic acid = Released from the phospholipid membrane by phospholipase A2</p> Signup and view all the answers

    Match the components of acute inflammation with their characteristics:

    <p>Neutrophils = First responders to infection and tissue necrosis Edema = Swelling caused by fluid leakage NF-κB = Transcription factor activated by TLRs Mast cells = Release mediators such as histamine and arachidonic acid</p> Signup and view all the answers

    Match the following types of inflammation with their descriptions:

    <p>Acute inflammation = Immediate response to infection or tissue injury Chronic inflammation = Involves persistent inflammatory response Innate immunity = Non-specific immune response Adaptive immunity = Targets specific pathogens based on previous exposure</p> Signup and view all the answers

    Match the following immune cells with their associated functions:

    <p>Macrophages = Engulf and clear necrotic debris Dendritic cells = Present antigens to T lymphocytes Lymphocytes = Play a role in adaptive immunity Neutrophils = Participate in the elimination of pathogens</p> Signup and view all the answers

    Match the following components of the inflammatory response with their effects:

    <p>PGE2 = Mediates pain and fever LTB4 = Chemotactic factor for neutrophils Cyclooxygenase = Enzyme that converts arachidonic acid to prostaglandins 5-lipoxygenase = Enzyme that produces leukotrienes</p> Signup and view all the answers

    Match the following terms related to inflammation with their definitions:

    <p>Pathogen-associated molecular patterns (PAMPs) = Molecules recognized by the innate immune system Exudate = Fluid with higher protein content that leaks into tissues Transudate = Fluid with lower protein content that leaks into tissues Anaphylatoxins = Molecules that mediate inflammation and increase vascular permeability</p> Signup and view all the answers

    Match the following inflammatory events with their mediators:

    <p>Vasodilation = Prostaglandins Neutrophil chemotaxis = Leukotrienes Endothelial cell contraction = Histamine Pain sensation = Bradykinin</p> Signup and view all the answers

    Match the following cytokines/mediators with their roles in inflammation:

    <p>TNF-α = Promotes systemic inflammation IL-1 = Induces fever and acute phase response IL-6 = Stimulates the production of acute phase proteins IL-8 = Recruits neutrophils to site of infection</p> Signup and view all the answers

    Study Notes

    Acute Inflammation

    • Characterized by the presence of edema and neutrophils in tissue.
    • Arises in response to infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris).
    • It is an immediate response with limited specificity (innate immunity).

    Mediators of Acute Inflammation

    • Toll-like receptors (TLRs): Present on innate immune system cells (macrophages, dendritic cells); activated by pathogen-associated molecular patterns (PAMPs) commonly shared by microbes.

      • CD14 - TLR4 co-receptor, recognizes lipopolysaccharide on gram-negative bacteria.
      • TLR activation: Upregulates NF-κB, a transcription factor activating immune response genes leading to multiple immune mediators.
      • TLRs are also present on adaptive immunity cells (e.g., lymphocytes) and play a role in chronic inflammation.

    • Arachidonic acid (AA) metabolites: Released from cell membrane by phospholipase A2.

      • Cyclooxygenase (COX): Produces prostaglandins (PG).
        • PGI2, PGD2, and PGE2 - Vasodilation and increased vascular permeability.
        • PGE2 - Pain and fever.
      • 5-lipoxygenase: Produces leukotrienes.
        • LTB4 - Attracts and activates neutrophils.
        • LTC4, LTD4, and LTE4 - Vasoconstriction, bronchospasm, increased vascular permeability.

    • Mast cells: Found in connective tissue.

      • Activated by:
        • Tissue trauma.
        • Complement proteins C3a and C5a.
        • Cross-linking of IgE by antigen.
      • Immediate response: Release of preformed histamine granules.
        • Vasodilation of arterioles and increased vascular permeability.
      • Delayed response: Production of arachidonic acid metabolites, particularly leukotrienes.

    • Complement: Proinflammatory serum proteins.

      • Circulate as inactive precursors; activation occurs through three pathways:
        • Classical pathway: C1 binds IgG or IgM bound to antigen.
        • Alternative pathway: Microbial products directly activate complement.
        • Mannose-binding lectin (MBL) pathway: MBL binds mannose on microorganisms and activates complement.
      • All pathways result in production of C3 convertase (mediates C3 → C3a and C3b) and C5 convertase (mediates C5 → C5a and C5b).
        • C5b complexes with C6-C9 to form the membrane attack complex (MAC).
        • C3a and C5a (anaphylatoxins) - Trigger mast cell degranulation leading to vasodilation and increased vascular permeability.
        • C5a - Chemotactic for neutrophils.
        • C3b - Opsonin for phagocytosis.
        • MAC - Lyses microbes by creating a hole in the cell membrane.

    • Hageman factor (Factor XII): Inactive proinflammatory protein, produced in the liver.

      • Activated upon exposure to subendothelial or tissue collagen; in turn activates:
        • Coagulation and fibrinolytic systems.
        • Complement.
        • Kinin system - Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin.
          • Bradykinin: Mediates vasodilation, increased vascular permeability (similar to histamine), and pain.

    Cardinal Signs of Inflammation

    • Redness (rubor) and warmth (calor): Due to vasodilation, increased blood flow.
      • Vasodilation occurs through relaxation of arteriolar smooth muscle; key mediators are histamine, prostaglandins, and bradykinin.
    • Swelling (tumor): Due to leakage of fluid from postcapillary venules into the interstitial space - exudate.
      • Key mediators are:
        • Histamine - Causes endothelial cell contraction.
        • Tissue damage - Results in endothelial cell disruption.
    • Pain (dolor):
      • Bradykinin and PGE2 sensitize sensory nerve endings.

    Inflammation

    • Inflammation is a complex biological response of vascular tissue to harmful stimuli, such as pathogens, damaged cells, or irritants
    • It involves immune cells, blood vessels, and molecular mediators that work together to eliminate the stimulus, repair damaged tissue, and restore homeostasis

    Acute Inflammation

    • Acute inflammation is the initial response to injury or infection.
    • Neutrophils, a type of white blood cell, are the primary inflammatory cells involved in acute inflammation.
    • Edema, accumulation of fluid in the interstitial space, is a characteristic feature of acute inflammation

    Mediators of Acute Inflammation

    • Toll-like receptors (TLRs) on immune cells (macrophages, dendritic cells) recognize pathogen-associated molecular patterns (PAMPs) found on microbes.
      • TLR activation triggers the production of inflammatory mediators.
    • Arachidonic acid (AA) metabolites are also key mediators of inflammation.
      • Prostaglandins (PG): PGI2, PGD2, and PGE2 cause vasodilation and increased vascular permeability. PGE2 also mediates pain and fever.
      • Leukotrienes (LT): LTB4 attracts and activates neutrophils. LTC4, LTD4, and LTE4 (slow reacting substances of anaphylaxis) constrict blood vessels, cause bronchospasm, and increase vascular permeability.
    • Mast cells are abundant in connective tissue and play a crucial role in acute inflammation. They release histamine and other inflammatory mediators.
      • Histamine causes vasodilation and increased vascular permeability.
    • Complement is a system of serum proteins that amplify the inflammatory response.
      • Activation pathways: Classical, alternative, and lectin pathways.
      • Functions: Activates other mediators, opsonizes microbes, and directly kills pathogens.
    • Hageman factor (Factor XII) is activated upon exposure to collagen.
      • Functions: Activates coagulation, fibrinolysis, complement, and the kinin system.

    Cardinal Signs of Inflammation

    • Redness (rubor) and warmth (calor)
      • Caused by vasodilation and increased blood flow.
    • Swelling (tumor)
      • Caused by fluid leakage from blood vessels into the interstitial space.
    • Pain (dolor)
      • Mediated by inflammatory mediators, such as bradykinin and prostaglandins, which sensitize nerve endings.
    • Loss of function (functio laesa)
      • This may occur as a result of pain, swelling, or tissue damage.

    Inflammation

    • Involves inflammatory cells, plasma proteins, and fluid exiting blood vessels and entering interstitial space
    • Divided into acute and chronic inflammation

    Acute Inflammation

    • Characterized by edema and neutrophils in tissue
    • Occurs in response to infection or tissue necrosis
    • Immediate and non-specific immune response (innate immunity)

    Mediators of Acute Inflammation

    • Toll-like receptors (TLRs)
      • Present on innate immune cells (e.g., macrophages and dendritic cells)
      • Activated by pathogen-associated molecular patterns (PAMPs) shared by microbes
        • CD14 recognizes lipopolysaccharide (PAMP) on gram-negative bacteria
      • TLR activation upregulates NF-κB, a nuclear transcription factor that activates immune response genes
      • TLRs also present on adaptive immune cells (e.g., lymphocytes) and play a role in chronic inflammation
    • Arachidonic acid (AA) metabolites
      • AA released from cell membrane by phospholipase A2
      • Metabolized by cyclooxygenase or 5-lipoxygenase
        • Cyclooxygenase produces prostaglandins (PG)
          • PGI2, PGD2, and PGE2 mediate vasodilation and increased vascular permeability
          • PGE2 also mediates pain and fever
        • 5-lipoxygenase produces leukotrienes (LT)
          • LTB4 attracts and activates neutrophils
          • LTC4, LTD4, and LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, bronchospasm, and increased vascular permeability
    • Mast cells
      • Widely distributed in connective tissue
      • Activated by tissue trauma, complement proteins C3a and C5a, or cross-linking of cell-surface IgE by antigen
        • Immediate response: release of preformed histamine granules, leading to vasodilation and increased vascular permeability
        • Delayed response: production of arachidonic acid metabolites, particularly leukotrienes
    • Complement
      • Proinflammatory serum proteins that enhance inflammation
      • Circulate as inactive precursors; activation occurs through:
        • Classical pathway: C1 binds IgG or IgM bound to antigen
        • Alternative pathway: Microbial products directly activate complement
        • Mannose-binding lectin (MBL) pathway: MBL binds to mannose on microorganisms
      • All pathways lead to production of C3 convertase (C3 → C3a and C3b), which produces C5 convertase (C5 → C5a and C5b)
      • C5b complexes with C6-C9 to form the membrane attack complex (MAC)
        • C3a and C5a (anaphylatoxins) trigger mast cell degranulation, resulting in histamine-mediated vasodilation and increased vascular permeability
        • C5a is chemotactic for neutrophils
        • C3b is an opsonin for phagocytosis
        • MAC lyses microbes by creating a hole in the cell membrane
    • Hageman factor (Factor XII)
      • Inactive proinflammatory protein produced in the liver
      • Activated upon exposure to subendothelial or tissue collagen
      • Activates:
        • Coagulation and fibrinolytic systems
        • Complement
        • Kinin system: Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin, which mediates vasodilation, increased vascular permeability, and pain

    Cardinal Signs of Inflammation

    • Redness (rubor) and warmth (calor)
      • Due to vasodilation, resulting in increased blood flow
      • Caused by relaxation of arteriolar smooth muscle, mediated by histamine, prostaglandins, and bradykinin
    • Swelling (tumor)
      • Leakage of fluid from postcapillary venules into the interstitial space (exudate)
      • Key mediators are histamine, which causes endothelial cell contraction, and tissue damage, resulting in endothelial cell disruption
    • Pain (dolor)
      • Bradykinin and PGE2 sensitize sensory nerve endings

    Inflammation

    • A complex process that allows immune cells, proteins, and fluids to move from blood vessels into tissues.
    • Two types of inflammation: Acute and Chronic

    Acute Inflammation

    • Characterized by edema and neutrophils in the tissue.
    • Occurs in response to infection or tissue damage.
    • A rapid response with limited specificity (innate immunity).
    • Key mediators include:

      • Toll-like receptors (TLRs)

        • Present on innate immune cells (macrophages, dendritic cells).
        • Activated by pathogen-associated molecular patterns (PAMPs) on microbes.
        • TLR activation triggers NF-κB, a transcription factor that regulates inflammatory responses.
        • TLRs also play a role in chronic inflammation.

      • Arachidonic acid (AA) metabolites

        • Generated from phospholipid cell membrane by phospholipase A2.
        • Metabolized by either cyclooxygenase or 5-lipoxygenase.
        • Cyclooxygenase produces prostaglandins (PG):
          • PGI 2, PGD 2, and PGE2 mediate vasodilation and vascular permeability.
          • PGE2 also mediates pain and fever.
        • 5-lipoxygenase produces leukotrienes (LT):
          • LTB 4 attracts and activates neutrophils.
          • LTC 4, LTD 4, and LTE 4 (slow reacting substances of anaphylaxis) cause vasoconstriction, bronchospasm, and increased vascular permeability.

      • Mast cells

        • Found in connective tissue.
        • Activated by trauma, complement proteins C3a and C5a, or cross-linking of cell-surface IgE by antigen.
        • Immediate response involves release of histamine granules, which mediate vasodilation of arterioles and increased vascular permeability.
        • Delayed response involves the production of arachidonic acid metabolites, particularly leukotrienes.

      • Complement

        • Proinflammatory serum proteins.
        • Circulate as inactive precursors.
        • Three activation pathways:
        • Classical: C1 binds IgG or IgM that is bound to antigen.
        • Alternative: Microbial products directly activate complement.
        • Mannose-binding lectin (MBL): MBL binds to mannose on microorganisms and activates complement.
        • All pathways lead to the production of C3 convertase (mediates C3 →C3a and C3b) and C5 convertase (mediates C5 → C5a and C5b).
        • C5b complexes with C6-C9 to form the membrane attack complex (MAC).
        • Complement functions:
        • C3a and C5a (anaphylatoxins): trigger mast cell degranulation resulting in histamine-mediated vasodilation and increased vascular permeability.
        • C5a: chemotactic for neutrophils.
        • C3b: opsonin for phagocytosis.
        • MAC: lyses microbes by creating a hole in the cell membrane.

      • Hageman factor (Factor XII)

        • Inactive proinflammatory protein produced in liver.
        • Activated upon exposure to subendothelial or tissue collagen.
        • Activates: coagulation and fibrinolytic systems, complement, and the kinin system.
        • Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin.
        • Bradykinin mediates vasodilation and increased vascular permeability (similar to histamine) and also causes pain.

    Cardinal Signs of Inflammation

    • Redness (rubor) and warmth (calor)
      • Result from vasodilation, which increases blood flow.
      • Mediated by histamine, prostaglandins, and bradykinin.
    • Swelling (tumor)
      • Caused by leakage of fluid from post-capillary venules into the interstitial space (exudate).
      • Key mediators are histamine, which causes endothelial cell contraction, and direct tissue damage, which disrupts endothelial cells.
    • Pain (dolor)
      • Bradykinin and PGE2 sensitize sensory nerve endings.

    Inflammation

    • Characterized by edema and neutrophils in tissue
    • Occurs in response to infection or tissue necrosis
    • A rapid but non-specific response (innate immunity)

    Acute Inflammation Mediators

    • Toll-like receptors (TLRs)
      • Present on immune cells (macrophages, dendritic cells)
      • Activated by pathogen-associated molecular patterns (PAMPs), found commonly in microbes
        • CD14 on macrophages recognizes lipopolysaccharide (LPS), a PAMP on gram-negative bacteria
      • Activation leads to NF-κB upregulation, triggering immune response genes and production of mediators
      • Present on lymphocytes and play a role in chronic inflammation
    • Arachidonic acid (AA) metabolites:
      • AA released from phospholipid membrane by phospholipase A2
      • Processed by cyclooxygenase or 5-lipoxygenase
        • Cyclooxygenase produces prostaglandins (PG):
          • PGI2, PGD2, and PGE2 mediate vasodilation and increased vascular permeability
          • PGE2 also causes pain and fever
        • 5-lipoxygenase produces leukotrienes (LT):
          • LTB4 attracts and activates neutrophils
          • LTC4, LTD4, and LTE4 (slow-reacting substances of anaphylaxis) mediate vasoconstriction, bronchospasm, and increased vascular permeability
    • Mast cells:
      • Distributed throughout connective tissue
      • Activated by:
        • Tissue trauma
        • Complement proteins C3a and C5a
        • IgE cross-linking by antigen
      • Immediate response: release of histamine, causing vasodilation and increased vascular permeability
      • Delayed response: production of AA metabolites, particularly leukotrienes
    • Complement:
      • Proinflammatory serum proteins that enhance inflammation
      • Inactive precursors activated through three pathways:
        • Classical pathway: C1 binds to IgG/IgM bound to antigen
        • Alternative pathway: Microbial products directly activate complement
        • Mannose-binding lectin (MBL) pathway: MBL binds to mannose on microorganisms, activating complement
      • All pathways produce C3 convertase , which then produces C5 convertase
        • C3a and C5a (anaphylatoxins): trigger mast cell degranulation, causing vasodilation and increased vascular permeability
        • C5a: chemotactic for neutrophils
        • C3b: opsonizes for phagocytosis
        • C5b complex (MAC): lyses microbes by forming a hole in the cell membrane
    • Hageman factor (Factor XII):
      • Inactive proinflammatory protein produced in the liver
      • Activated upon exposure to collagen, activating:
        • Coagulation and fibrinolytic systems
        • Complement
        • Kinin system: Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin, causing vasodilation, increased vascular permeability (similar to histamine) and pain

    Cardinal Signs of Inflammation

    • Redness (rubor) and warmth (calor)
      • Caused by vasodilation, increasing local blood flow
      • Mediated by histamine, prostaglandins, and bradykinin
    • Swelling (tumor):
      • Due to fluid leakage from postcapillary venules into the interstitial space (exudate)
      • Key mediators are histamine, causing endothelial cell contraction, and tissue damage, leading to endothelial cell disruption
    • Pain (dolor):
      • Bradykinin and PGE2 sensitize sensory nerve endings

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    Inflammation, Inflammatory Disorders, and Wound Healing PDF

    Description

    Test your knowledge on acute inflammation, including its characteristics and role in immune response. Explore key mediators such as Toll-like receptors and arachidonic acid metabolites that play a vital role in combating infection and tissue damage.

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