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Questions and Answers
What is the role of laminar flow in leukocyte recruitment?
What is the role of laminar flow in leukocyte recruitment?
Which of the following is NOT a factor that accelerates contact between leukocytes and endothelial cells?
Which of the following is NOT a factor that accelerates contact between leukocytes and endothelial cells?
How do integrins contribute to leukocyte recruitment?
How do integrins contribute to leukocyte recruitment?
What is the function of selectins in leukocyte recruitment?
What is the function of selectins in leukocyte recruitment?
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What is the significance of relative speed in leukocyte recruitment?
What is the significance of relative speed in leukocyte recruitment?
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Which of the following is the correct order of events in leukocyte recruitment?
Which of the following is the correct order of events in leukocyte recruitment?
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Which of the following molecules is NOT a primary mediator of vascular permeability?
Which of the following molecules is NOT a primary mediator of vascular permeability?
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What is the main function of the inflammasome in the inflammatory response?
What is the main function of the inflammasome in the inflammatory response?
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What is a potential therapeutic strategy based on the mechanisms of leukocyte recruitment?
What is a potential therapeutic strategy based on the mechanisms of leukocyte recruitment?
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How does stasis contribute to leukocyte recruitment?
How does stasis contribute to leukocyte recruitment?
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Which of the following is NOT a characteristic of cytokines?
Which of the following is NOT a characteristic of cytokines?
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What is the primary function of the kinin cascade in inflammation?
What is the primary function of the kinin cascade in inflammation?
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What is the most likely outcome of increased vascular permeability during inflammation?
What is the most likely outcome of increased vascular permeability during inflammation?
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What is the primary role of neutrophils in the inflammatory response?
What is the primary role of neutrophils in the inflammatory response?
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What is the difference between the immediate transient response and the slower, prolonged retraction of endothelial cells in inflammation?
What is the difference between the immediate transient response and the slower, prolonged retraction of endothelial cells in inflammation?
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What is the role of Hageman factor in the inflammatory response?
What is the role of Hageman factor in the inflammatory response?
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Which of the following is NOT a major component of acute inflammation?
Which of the following is NOT a major component of acute inflammation?
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What is the primary function of complement proteins in inflammation?
What is the primary function of complement proteins in inflammation?
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Which of the following cytokines promote the expression of selectins and integrin ligands on endothelium?
Which of the following cytokines promote the expression of selectins and integrin ligands on endothelium?
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Which type of tissue is capable of regenerating after injury due to its quiescent state and potential for proliferation?
Which type of tissue is capable of regenerating after injury due to its quiescent state and potential for proliferation?
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What is the primary component of fibrous connective tissue that builds up in the process of fibrosis?
What is the primary component of fibrous connective tissue that builds up in the process of fibrosis?
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Which of the following signaling pathways involves communication between cells in a local area, affecting cells in close proximity?
Which of the following signaling pathways involves communication between cells in a local area, affecting cells in close proximity?
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What is the primary function of Extracellular Matrix (ECM) in wound healing?
What is the primary function of Extracellular Matrix (ECM) in wound healing?
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What is the main function of the acute phase response in the context of inflammation?
What is the main function of the acute phase response in the context of inflammation?
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Which of the following is NOT a function of Extracellular Matrix (ECM)?
Which of the following is NOT a function of Extracellular Matrix (ECM)?
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What is the term for the process where pathogens are marked for destruction by phagocytes?
What is the term for the process where pathogens are marked for destruction by phagocytes?
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Which of the following accurately describes Disseminated Intravascular Coagulation (DIC)?
Which of the following accurately describes Disseminated Intravascular Coagulation (DIC)?
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Which of the following tissues is considered Permanent tissue, incapable of regeneration?
Which of the following tissues is considered Permanent tissue, incapable of regeneration?
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What is the primary role of C-reactive protein (CRP) in the immune response?
What is the primary role of C-reactive protein (CRP) in the immune response?
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What is the difference between regeneration and resolution in tissue repair?
What is the difference between regeneration and resolution in tissue repair?
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Which of the following is NOT a factor that influences tissue repair?
Which of the following is NOT a factor that influences tissue repair?
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Which of these would NOT be considered a systemic effect of inflammation?
Which of these would NOT be considered a systemic effect of inflammation?
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Which of these mediators is primarily responsible for killing microbes?
Which of these mediators is primarily responsible for killing microbes?
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Which mediator is known for its potent vasodilation and increased vascular permeability, even exceeding the potency of histamine?
Which mediator is known for its potent vasodilation and increased vascular permeability, even exceeding the potency of histamine?
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Which of the following is NOT a direct action of Nitric Oxide?
Which of the following is NOT a direct action of Nitric Oxide?
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What is the primary source of cytokines in the inflammatory process?
What is the primary source of cytokines in the inflammatory process?
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Which type of cytokine is primarily involved in activating endothelial cells, leading to leukocyte adhesion?
Which type of cytokine is primarily involved in activating endothelial cells, leading to leukocyte adhesion?
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Which of these is NOT a characteristic of the inflammasome?
Which of these is NOT a characteristic of the inflammasome?
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Which of the following mediator is known for being a derivative of arachidonic acid?
Which of the following mediator is known for being a derivative of arachidonic acid?
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Which of the following mediators is NOT a polypeptide or small protein?
Which of the following mediators is NOT a polypeptide or small protein?
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How does the inflammasome activate inflammatory responses?
How does the inflammasome activate inflammatory responses?
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Which of the following mediators is responsible for killing microbes by reducing oxidative burst?
Which of the following mediators is responsible for killing microbes by reducing oxidative burst?
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Flashcards
Serotonin
Serotonin
A vasoactive amine released in inflammation.
Prostaglandins
Prostaglandins
Mediators from mast cells and leukocytes causing vasodilation, pain, and fever.
Leukotrienes
Leukotrienes
Mediators that increase vascular permeability and help in leukocyte functions.
Platelet-Activating Factor (PAF)
Platelet-Activating Factor (PAF)
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Reactive Oxygen Species (ROS)
Reactive Oxygen Species (ROS)
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Nitric Oxide
Nitric Oxide
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Cytokines
Cytokines
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Lymphokines
Lymphokines
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Inflammasome
Inflammasome
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Cytokine Network
Cytokine Network
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Laminar Flow
Laminar Flow
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Relative Speed
Relative Speed
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Stasis
Stasis
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Integrins
Integrins
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Selectins
Selectins
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Diapedesis
Diapedesis
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Rolling
Rolling
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Chemotaxis
Chemotaxis
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Pro-inflammatory cytokines
Pro-inflammatory cytokines
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Pleiotropy of cytokines
Pleiotropy of cytokines
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Cytokine redundancy
Cytokine redundancy
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Inflammatory exudate
Inflammatory exudate
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Vascular permeability
Vascular permeability
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Leukocyte emigration
Leukocyte emigration
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Complement system
Complement system
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Kinin cascade
Kinin cascade
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Endothelial cell contraction
Endothelial cell contraction
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Cell Proliferation
Cell Proliferation
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Labile Tissues
Labile Tissues
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Stable Tissues
Stable Tissues
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Permanent Tissues
Permanent Tissues
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Extracellular Matrix (ECM)
Extracellular Matrix (ECM)
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Leukocyte Recruitment
Leukocyte Recruitment
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Firm Attachment
Firm Attachment
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Chemokines
Chemokines
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Phagocytosis
Phagocytosis
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Acute Inflammation
Acute Inflammation
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Chronic Inflammation
Chronic Inflammation
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Fibrosis
Fibrosis
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Acute Phase Response
Acute Phase Response
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Acute Phase Proteins (APPs)
Acute Phase Proteins (APPs)
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C-reactive protein (CRP)
C-reactive protein (CRP)
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Regeneration
Regeneration
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Healing with Scar Formation
Healing with Scar Formation
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Tissue Repair Factors
Tissue Repair Factors
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Study Notes
Inflammation Overview
- Inflammation is a Latin word, "inflammatio", meaning "setting on fire"
- It is a protective response to eliminate the cause of injury or necrotic cells
- The process neutralizes harmful agents and initiates healing
- Inflammation can be acute or chronic
Learning Objectives
- Describe the general features and mechanisms of inflammation
- Describe the role of principal mediators in inflammation
- Describe vascular and cellular events associated with inflammation
- Distinguish between acute and chronic inflammation
Hallmarks of Acute Inflammation
- Redness
- Heat (increased temperature)
- Swelling (edema)
- Pain
- Loss of function
The Pillars of Inflammation
- Described by Aulus Cornelius Celsus (over 2000 years ago)
- Include: redness, swelling, heat, pain, loss of function
Inflammation: Friend or Foe?
- Inflammation is a protective response to injury and/or necrotic cells
- Inflammation can cause harm to healthy tissue
Mediators of Inflammation
- Produced locally or circulating in plasma as inactive precursors activated at the site of inflammation
- Induce effects by binding target cells (except ROS and some proteases)
- Prime targets for anti-inflammatory drugs
Major Players in Inflammation
- Mast cells
- Macrophages
- Platelets
- Lymphocytes
- Monocytes
- Polymorphonuclear leukocytes
- Plasma proteins
- Fibroblasts
- Complement
- Clotting factors/kininogens
Chemical Mediators of Inflammation
- Produced locally within cells at the site of inflammation, or within the plasma
- May include histamine, serotonin, prostaglandins, leukotrienes, platelet-activating factor (PAF), reactive oxygen species(ROS), nitric oxide, and Cytokines
Mediator Summaries
- Histamine: increased vascular permeability, vasodilation
- Serotonin: increased vascular permeability, vasodilation
- Prostaglandins: vasodilation, pain, fever
- Leukotrienes: increased vascular permeability, chemotaxis, leukocyte adhesion/activation
- Platelet-activating factor(PAF): vasodilation, increased vascular permeability, leukocyte activation, etc.
- Reactive oxygen species (ROS): killing of microbes
- Nitric oxide: vasodilation, reduced leukocyte adhesion
- Cytokines: Local endothelial activation, chemotaxis, leukocyte activation, systemic effects.
Cytokines
- Polypeptides/small proteins released from cells to interact with and communicate with each other
- Types of cytokines includes lymphokines(lymphocyte produced), monokines (monocyte produced), chemokines (chemotactic activities), interleukins, and interferons.
- Cytokines involved in systemic inflammation are tumor necrosis factors.
Cytokine Signaling
- Autocrine: Cell signals itself
- Paracrine: Cell signals neighboring cell
- Endocrine: Cell signals distant cell through blood circulation
Inflammasome
- Cytosolic multiprotein complex
- Activates inflammatory responses
- Promotes maturation and secretion of pro-inflammatory cytokines (IL-1 and IL-18)
T-Helper Cells and Regulation
- Pro-inflammatory cytokines (e.g., IL-1β, IL-6, IL-23, TNF-α by Th17) mediate inflammation
- Regulated by anti-inflammatory cytokines produced by regulatory T cells (e.g., IL-10, TGF-β).
Acute Phase Response
- Non-specific indicators of inflammation
- Systemic effects of inflammation
- Production of acute-phase proteins (e.g., fibrinogen and CRP), etc.
- Symptoms include fever, anorexia, malaise, somnolence, and leukocytosis.
- Includes factors that cause shock such as high TNF & IL-1, DIC (disseminated intravascular coagulation)
- Results in high levels of acute-phase proteins (like CRP) and increased production of leukocytes in the bone marrow
Acute Phase Proteins (APPs)
- Large group of biochemically and functionally unrelated proteins
- Plasma concentrations increase or decrease in response to tissue injury, acute infections, burns or chronic inflammation
- Examples include CRP, serum amyloid protein
Wound Healing and Tissue Repair
- Tissue repair = regeneration (complete functional replacement) or resolution
- Tissue repair depends on cell proliferation, extracellular growth factors and ECM (extracellular matrix)`
Cell Proliferation
- Labile tissues – continuously dividing (e.g., hematopoietic cells, GI tract epithelia)
- Stable tissues – quiescent but can proliferate (e.g. liver, pancreas)
- Permanent tissues – terminally differentiated and non-proliferative (e.g. neurons, cardiac muscle cells)
Extracellular Growth Factors
- Signaling molecules that stimulate cell proliferation, movement, and differentiation
- Types of growth factors include platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-B).
Extracellular Matrix (ECM)
- Complex network that surrounds cells
- ECM sequesters water, provides mechanical stability, a substrate for cell adhesion.
- Provides a scaffolding structure for tissue renewal
- Acts as a reservoir of growth factors
Tissue Repair: Wound Healing
- Healing can occur via first intention or second intention
- In first-intention healing, there is only minimal injury or damage
- Second-intention healing occurs when there is more extensive damage
Granulation Tissue
- Composed of inflammatory cells and fibroblasts
- Granulation tissue forms during wound healing, and is composed of blood vessels
Chronic Inflammation
- Lasting weeks, months or years
- Characterized by tissue damage
- Involves continuous activation of macrophages, angiogenesis, and fibrosis
Systemic effects of inflammation
- Describes fever, malaise, or other non-specific indicators that might indicate inflammation
- Non-specific markers of inflammation include ESR (Erythrocyte Sedimentation Rate).
Leukocyte-induced tissue injury
- Caused by ROS, RNS, enzymes that act on surrounding tissues not just solely on the original invaders
- Occurs in autoimmune diseases, allergic reaction, and other conditions.
Clinical examples of inflammation
- Includes respiratory, transplant, glomerulonephritis、septic sock, and vasculitis; arthritis, atherosclerosis, transplant rejection, and pulmonary fibrosis; acute and chronic inflammation
Fibrosis
- Excessive scarring exceeding typical wound healing
- Can also be a normal healing response (such as with a wound) or occur as a pathologic response (disease)
Inflamed Capillary Bed
- Shows increased blood flow within capillaries
- Shows leakage of plasma proteins as edema occurs
- Shows migration and accumulation of leukocytes at the site of the injury
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Description
Test your knowledge on the mechanisms involved in leukocyte recruitment, including the roles of laminar flow, selectins, and integrins. This quiz explores key factors that influence leukocyte movement and their interactions with endothelial cells during inflammation. Understand the significance of these processes in immune responses and potential therapeutic strategies.