Questions and Answers
Which of the following adhesion molecules is primarily responsible for the migration of lymphocytes to the gut and gut-associated lymphoid tissues?
Which of the following is NOT a ligand for L-selectin?
Which of the following adhesion molecules is expressed on activated endothelium and plays a critical role in the adhesion of neutrophils, monocytes, and T lymphocytes?
Which of the following adhesion molecules is primarily responsible for the adhesion of monocytes and dendritic cells to activated endothelium?
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Which of the following statements accurately describes the expression of integrins on leukocytes?
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Which of the following adhesion molecules is NOT expressed on activated endothelium?
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Which of the following adhesion molecules is primarily responsible for the adhesion of T lymphocytes to activated endothelium?
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Which of the following adhesion molecules plays a role in the extravasation of leukocytes from the bloodstream into tissues?
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What role do activated neutrophils play in the immune response?
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Which of the following is NOT a mechanism by which neutrophils alter the concentration of integrins?
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What happens to particles that are wrapped by neutrophil membranes?
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Which statement best describes the significance of neutrophil signaling to macrophages?
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Which type of particles can neutrophils engulf and internalize?
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How do neutrophils engage with debris or foreign particles?
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What is the predominant type of cell that dominates during the first 6 to 24 hours of acute vascular damage?
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What physiological condition describes red blood cells stuck in small vessels resulting in localized swelling?
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What process do red blood cells undergo 24 to 48 hours after acute injury?
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What visible sign is associated with localized redness due to vascular congestion?
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Which cellular component primarily replaces red blood cells after they undergo apoptosis?
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What occurs during vascular congestion that contributes to the phenomenon of 'swelling'?
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When does the process of leukocyte margination occur in relation to acute vascular injury?
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During which phase do neutrophils begin to adhere to the vascular endothelium?
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What is a consequence of processes that give rise to LTB or LTC?
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Which of the following best describes LTB?
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What type of mechanisms may develop when inflammation is abnormally charged?
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What role do macrophages play in the context of neuroinflammation?
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Which process is primarily responsible for the release of lysosomal enzymes in inflammation?
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What can trigger the aggregation and adhesion of antigens during inflammation?
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Which statement correctly reflects the outcome of neuroinflammatory responses?
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What do elevated levels of ROS commonly contribute to?
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What is the primary function of histamine in the context of reactive oxygen species (ROS) generation?
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Which enzyme is primarily involved in the production of superoxide during the activation of mast cells?
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Under what conditions is hydrogen peroxide generated in relation to mast cells and signaling?
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What role do Fc receptors play in the context of mast cell activation?
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How do reactive oxygen species contribute to tissue damage?
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What is the effect of complement products C5a and C3a on mast cell activity?
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Which of the following statements about enzyme activities in mast cells is true?
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What is the significance of rapid assembly in the context of phagocyte oxidase?
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Neutrophils are responsible for recognizing and responding to microbial invasion.
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Tissue cells can recognize and respond to microbial invasion without the help of neutrophils.
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Proteins are the primary molecules responsible for recognizing and responding to microbial invasion.
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Neutrophils can engulf and internalize foreign particles through a process called phagocytosis.
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Neutrophils are not capable of recognizing foreign particles in the absence of complement proteins.
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The primary function of neutrophils is to produce antibodies against invading pathogens.
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Neutrophils are the primary cells responsible for the resolution of inflammation.
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Inflammation is always a beneficial response to tissue damage or infection.
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The principal cells of inflammation are erythrocytes.
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Cytokines are the primary mediators of acute inflammation.
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Macrophages are the primary cellular infiltrate in acute inflammation.
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Chronic inflammation is typically self-limited.
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Pyogenic bacteria are a common cause of chronic inflammation.
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Leukocytes express receptors for the Fc portion of antibodies.
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Tissue injury is usually extensive in acute inflammation.
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Scarring is a common outcome of acute inflammation.
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Cytokines are involved in the production of prostaglandins and leukotrienes.
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Local and systemic signs of inflammation are usually mild in chronic inflammation.
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Neutrophils have a life span in tissues of approximately 1–2 years.
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Macrophages are primarily derived from hematopoietic stem cells found in the yolk sac or fetal liver during early development.
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The response of neutrophils to activating stimuli is typically slower and dependent on new gene transcription.
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Cytokine production is a major response feature of neutrophils.
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Degranulation is a prominent response in macrophages when activated.
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Reactive oxygen species are less prominently induced in neutrophils compared to macrophages.
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Both neutrophils and macrophages have a significant capacity for NET formation.
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Nitric oxide is typically present at low levels or none in neutrophils.
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Secretion of lysosomal enzymes is more prominent in macrophages than in neutrophils.
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Macrophages rely on rapid, short-lived responses similar to neutrophils when activated.
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H$_2$O can be converted to highly reactive hydroxyl radicals (OH) in the presence of metals such as Al.
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Microbicidal reactive oxygen species (ROS) and nitrogen oxides are essential for killing ingested microbes.
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Inducible NO synthase (iNOS) is only produced during the resting state of phagocytes.
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Phagocytes use endosomes to capture and ingest microbial particles.
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Mannose receptors are examples of mediators that phagocytes utilize to bind to microbes.
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Nitric oxide (NO) released during phagocytosis can contribute to inhibiting microbial growth.
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Reactive oxygen species (ROS) are exclusively produced in the presence of nitrogen oxides.
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Granule contents may be released into extracellular tissues during the process of phagocytosis.
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P-selectin is a type of integrin involved in stable adhesion of leukocytes.
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Fibrin and fibronectin are components of the extracellular matrix that assist in leukocyte migration.
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Chemokines play a critical role in integrating the low-affinity state of integrins to a high-affinity state in leukocytes.
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Leukocyte rolling is primarily mediated by the interaction of integrins with endothelial cells.
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PECAM-1 is also known as CD31 and plays a role in the migration of leukocytes through the endothelium.
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The activation of integrins in leukocytes occurs independently of cytokines like TNF and IL-1.
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Cytokines and chemokines are interchangeable terms in the context of leukocyte activation.
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Microbial presence triggers a defensive response from macrophages through chemokines and integrins.
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What is the primary consequence of chronic inflammation compared to acute inflammation?
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What is the role of sensors in the context of inflammation?
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What is the primary difference between the vascular and cellular reactions in inflammation?
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What is the primary function of chemical mediators in inflammation?
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What is the significance of de novo synthesis in the context of acute and chronic inflammation?
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What is the primary role of cytokines in the context of inflammation?
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What is the primary consequence of uncontrolled inflammation?
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What is the significance of the distinction between acute and chronic inflammation?
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What specific adhesion molecule plays a critical role in the migration of T lymphocytes to gut and gut-associated lymphoid tissues?
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Which adhesion molecule is primarily responsible for the adhesion of neutrophils, monocytes, and T lymphocytes to activated endothelium?
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What is the ligand for LFA-1 integrin on activated endothelium?
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Which adhesion molecule is expressed on monocytes and dendritic cells and plays a role in their adhesion to activated endothelium?
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What is the primary ligand for VLA-4 integrin on T lymphocytes?
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Which adhesion molecule is responsible for the adhesion of neutrophils and monocytes to activated endothelium?
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What is the ligand for α4β7 integrin on T lymphocytes and monocytes?
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Which family of adhesion molecules is responsible for the rolling of leukocytes on endothelium?
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What is the primary mechanism by which cell-derived mediators acquire the ability to destroy ingested microbes and dead cells?
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What is the role of lysosomal enzymes in the context of inflammation?
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How do neutrophils engage with debris or foreign particles?
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What is the significance of elevated levels of reactive oxygen species (ROS) in inflammation?
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What is the primary function of histamine in the context of reactive oxygen species (ROS) generation?
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What is the role of Fc receptors in the context of mast cell activation?
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Explain how the lymphatic vessels and lymph nodes contribute to the inflammatory response, focusing on their roles in removing exudate and mediating the movement of leukocytes.
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Describe the mechanisms by which adhesion molecules facilitate the recruitment of leukocytes to the site of inflammation. Include specific examples of adhesion molecules and their functions.
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Explain the role of neutrophils in the early stages of acute inflammation, including their functions in phagocytosis, degranulation, and the production of reactive oxygen species (ROS).
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Discuss the mechanisms by which mast cells contribute to inflammation, including the release of histamine and other mediators, the activation of complement, and the production of reactive oxygen species (ROS).
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Describe the process of leukocyte margination and explain how it facilitates the extravasation of leukocytes into the inflamed tissue.
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Explain the role of macrophages in the resolution of inflammation, including their functions in phagocytosis, antigen presentation, and the release of cytokines.
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Describe the process by which activated neutrophils engulf and internalize foreign particles, highlighting the key steps involved.
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Explain how the interaction between activated neutrophils and macrophages contributes to the overall immune response.
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Describe the role of reactive oxygen species (ROS) in the inflammatory response, highlighting their beneficial and detrimental effects.
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Explain the concept of "phagocytosis" in the context of the immune response and its significance in eliminating foreign particles.
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Discuss the significance of "adhesion molecules" in the context of leukocyte migration during inflammation.
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Describe the process by which activated neutrophils trigger the release of lysosomal enzymes during inflammation, and explain the consequences of this release.
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When pathogens invade the body, _______________ microbes are activated to fight the infection.
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The production of mediators requires the _______________ of blood vessels.
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Rapid changes in _______________ vessel walls are essential for the production of mediators.
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The exodus of cells from the _______________ into the surrounding tissue is crucial for the inflammatory response.
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Coordinated changes in _______________ vessels and the secretion of mediators are necessary for the inflammatory response.
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The _______________ of blood vessels is critical for the migration of leukocytes to the site of inflammation.
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The production of mediators is dependent on the _______________ of blood vessels and the secretion of pro-inflammatory molecules.
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The inflammatory response involves the _______________ of leukocytes from the bloodstream into the surrounding tissue.
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The ______ activation by chemokines plays a critical role in leukocyte migration.
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______ are a type of adhesion molecule that bind to specific ligands on leukocytes.
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The process of leukocyte movement through the endothelium is called ______.
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The ______ state of integrins refers to their low affinity for their ligands.
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The ______ of integrins enhances their binding to ligands on the endothelium.
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Cytokines such as TNF and IL-1 play a role in the ______ of the endothelium.
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______ are chemical messengers that attract leukocytes to the site of inflammation.
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The ______ matrix provides a scaffold for leukocyte migration.
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The process of engulfing foreign particles through the formation of a _______________ is shown in Fig.
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The _______________ is responsible for killing and degrading ingested microbes.
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Cytoplasmic _______________ is involved in the production of reactive oxygen species (ROS).
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The _______________ is an enzyme involved in the production of superoxide during the activation of phagocytes.
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The primary function of _______________ in phagocytes is to generate reactive oxygen species (ROS).
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The _______________ pathway is involved in the production of nitric oxide (NO) in phagocytes.
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The _______________ is formed when the phagosome fuses with a lysosome.
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Reactive oxygen species (ROS) contribute to _______________ during inflammation.
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The primary function of _______________ in phagocytes is to recognize and engulf foreign particles.
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The formation of _______________ around foreign particles is the first step in phagocytosis.
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Microbes and acid ______________ the cleanup of debris from necrotic cells.
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Prostaglandins and leukotrienes are derived from __________________ acid.
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Heavy issues are normally protected from ROS-mediated damage by the action of __________________ enzymes.
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The enzyme __________________ degrades superoxide, and catalase degrades hydrogen peroxide.
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Arachidonic acid is converted by the enzyme __________________ into prostaglandins and by lipoxygenase into leukotrienes.
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These chemicals have diverse actions on blood vessels and __________________ cells.
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Nitric oxide (NO) is made mostly in __________________ and following stimulation of macrophages.
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Reactive oxygen species (ROS) can cause __________________ damage to tissues.
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The major killing mechanisms of ______ and macrophages are produced locally by the sentinel cells.
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Reactive oxygen species (ROS) are classified as ______ that help in the destruction of pathogens.
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The mediators including chemokines and interferon-γ (IFN-γ) help to regulate mediatory actions such as those of ______ receptors.
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These mediators are crucial for destroying ______ and dead cells.
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Nitric oxide and enzymes are part of the major classes of ______ involved in the immune response.
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Mediators produced in response to infection contribute to a system of checks and balances that ______ immune actions.
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Match the following cellular structures with their functions:
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Match the following enzymes with their primary role in the production of reactive oxygen species (ROS) during inflammation:
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Match the following cell types with their primary role in the resolution of inflammation:
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Match the following molecules with their roles in eicosanoid production:
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Match the following processes with their primary role in the pathogenesis of chronic inflammation:
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Match the following enzymes with their roles in ROS degradation:
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Match the following processes with their effects during acute vascular damage:
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Match the following timeframes with the corresponding cellular responses during vascular damage:
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Match the following phases of leukocyte involvement with their characteristics:
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Study Notes
Acute Vascular Damage
- Acute vascular damage leads to reduced blood flow, heightened inflammation, and an increase in leukocyte concentration within 6 to 24 hours.
- Small blood vessels experience swelling, resulting in increased blood viscosity and the accumulation of red blood cells.
- This condition leads to a process known as stasis, marked by changes in the motion of blood and leukocytes, manifesting as localized redness (erythema) in affected areas.
Leukocyte Migration
- The migration of leukocytes can be divided into vascular congestion and external localized redness.
- Various types of leukocytes, including neutrophils and monocytes, adhere to the endothelium during the inflammatory process.
- Specific adhesion molecules, such as selectins and integrins, are crucial for leukocyte adherence and migration toward sites of inflammation.
Adhesion Molecules
-
Selectins: Facilitate initial leukocyte capture and rolling through interactions with sialyl-Lewis X on endothelial glycoproteins.
- L-selectin: Primarily found on lymphocytes.
- E-selectin: Detected on activated endothelium.
- P-selectin: Also on activated endothelium.
-
Integrins: Provide firm adhesion and promote transmigration of leukocytes across the endothelium.
- LFA-1 and MAC-1: Found on T lymphocytes and monocytes, interact with ICAM-1 on activated endothelium.
- VLA-4 and α4β7: Present on T lymphocytes and monocytes, bind to VCAM-1 and MAdCAM-1 on endothelium.
Inflammatory Cell Communication
- Activation of leukocytes occurs through receptors that signal from other immune cells like macrophages.
- ROS (Reactive Oxygen Species) production in neutrophils is enhanced, contributing to inflammation and phagocytosis of pathogens.
- Histamine increases vascular permeability and promotes tissue edema, aiding the recruitment of immune cells.
Consequences of Inflammation
- Excess activation of leukocytes can lead to tissue damage, which may exacerbate autoinflammatory responses.
- Increased levels of leukotrienes (LTB and LTC) result from neutrophils during inflammatory processes and can act as potent chemotactic agents.
- Aberrant immune responses may link to conditions such as allergic reactions or chronic inflammation, causing further damage to local tissues.
Summary
- Acute inflammation involves complex interactions between vascular responses, leukocyte adhesion, and signaling molecules, culminating in effective pathogen clearance but potential tissue damage if dysregulated.
Inflammation Overview
- Inflammation is a response to harmful stimuli such as microbes and necrotic tissue.
- Key mediators include opsonins, which label pathogens for destruction by immune cells.
Immune Cell Recruitment
- Recruitment of leukocytes and plasma proteins to sites of injury is crucial in inflammation.
- Tissue cells and blood circulation play vital roles in detecting and responding to inflammatory stimuli.
Principal Inflammatory Cells
- Major cell types include leukocytes, specifically neutrophils and macrophages.
- Neutrophils are the first responders, while macrophages play a prolonged role in healing and repairing tissues.
Acute vs Chronic Inflammation
-
Acute Inflammation:
- Rapid onset (minutes to hours) with a brief duration (days).
- Involves mainly neutrophils, usually self-limited tissue injury, and minimal scarring.
- Mediators include histamine, prostaglandins, and cytokines.
- Common causes include infections by pyogenic bacteria and viruses.
-
Chronic Inflammation:
- Slower onset (days) and prolonged duration.
- Involves macrophages, lymphocytes, and can cause extensive tissue damage and significant scarring.
- Mediators primarily consist of cytokines with less pronounced local and systemic signs.
Phagocytes
-
Neutrophils:
- Originate from hematopoietic stem cells in bone marrow.
- Short life span (1-2 days) in tissues and respond quickly to stimuli.
- Derived from degranulation and produce reactive oxygen species (ROS).
-
Macrophages:
- Can be derived from monocytes or early stem cells in the yolk sac or fetal liver during development.
- Long-lived, persisting in tissues for days, weeks, or even years.
- Play a role in prolonged inflammation and cytokine production.
Leukocyte Adhesion and Migration
- Leukocyte recruitment involves a sequence of rolling, integrin activation, stable adhesion, and migration through the endothelium.
- This process is mediated by selectins (P-selectin, E-selectin) and integrins which facilitate the attachment and movement across blood vessels.
Reactive Species in Phagocytosis
- Reactive oxygen species (ROS) and nitric oxide (NO) are crucial for killing ingested microbes.
- Different reactive species can harm both pathogens and host tissues if not carefully regulated.
Summary Table of Key Differences
- In acute inflammation: Neutrophils dominate, signs are prominent, and tissue injury is self-limited.
- In chronic inflammation: Macrophages and lymphocytes are prevalent, signs are milder, and tissue injury can be extensive and leading to scarring.
Role of Cytokines
- Cytokines like IL-1 play critical roles in mediating inflammation and activating immune responses.
- They are essential for communication between cells during inflammatory processes.
Inflammation Overview
- Inflammation triggers chemical mediators that facilitate vascular and cellular reactions to eliminate harmful agents.
- Chronic inflammation can develop after acute inflammation or evolve independently, characterized by prolonged duration.
Key Features of Chronic Inflammation
- Associated with increased tissue destruction compared to acute inflammation.
- Tissue damage may occur due to persistent presence of pathogens or inflammatory stimuli.
Cellular Components in Inflammation
- Inflammatory responses involve various immune cells:
- Cytokines: Critical signaling proteins released during inflammation.
- Macrophages and Lymphocytes: Key players in recognizing and responding to pathogens.
Mechanisms of Protective Response
- Activation of blood vessels enhances permeability, allowing essential immune components to access affected tissues.
- Lymphatic vessels play a role in draining exudate and transporting immune cells to lymph nodes.
Immune Cell Activation
- Functional distinctions exist between acute and chronic inflammation, driven by different cellular responses and mediators.
- Adhesion molecules mediate interactions between leukocytes and endothelial cells, facilitating migration to inflamed tissues.
Adhesion Molecules in Leukocyte Migration
-
Selectins:
- L-selectin on lymphocytes binds to sialyl-Lewis X on various glycoproteins.
- E-selectin and P-selectin on activated endothelium facilitate leukocyte adhesion through similar interactions with glycoproteins.
-
Integrins:
- Various integrins (e.g., LFA-1, MAC-1, VLA-4) are expressed on leukocytes, allowing firm adhesion to activated endothelial cells via their respective ligands (ICAM-1, VCAM-1).
Phagocytosis
- Neutrophils and macrophages engage in phagocytosis of pathogens, debris, and dead cells.
- Recognition of foreign particles occurs through receptors that activate and initiate engulfment.
- Pathogen-associated molecular patterns (PAMPs) trigger these immune mechanisms by binding receptors on phagocytes.
Mediators of Inflammation
- Reactive oxygen species (ROS) and nitric oxide produced by activated immune cells play prominent roles in pathogen destruction.
- Various mediators, such as cytokines and enzymes from lysosomes, facilitate inflammatory responses and tissue repair.
Conclusion on Inflammatory Responses
- The effectiveness of inflammation relies on a balanced action of mediators, ensuring that the response addresses pathogens without causing excessive tissue damage.
- Synchronization of processes involved in inflammation is crucial for a successful immune response.
Invasion and Production of Mediators
- Microbes can invade tissues, triggering a complex immune response.
- Key cells involved in this response include neutrophils, macrophages, and various leukocytes.
- Mediators such as cytokines and chemokines are essential for coordinating immune responses.
Blood Vessel Changes
- Inflammation causes blood vessels to change, facilitating the arrival of immune cells to the site of injury.
- Exudation of cells and plasma proteins from blood requires interrelated changes in blood vessel structures.
- Mediators released during this process lead to increased vascular permeability.
Rolling and Adhesion of Leukocytes
- Leukocyte rolling occurs due to interactions with P-selectin and E-selectin on endothelial cells.
- Integrin activation leads to stable adhesion of leukocytes, transitioning from a low-affinity to a high-affinity state.
- Chemokines play a vital role in integrin activation and subsequent migration of leukocytes through the endothelium.
Phagocytosis Mechanism
- Phagocytes engulf microbes, forming a phagosome that fuses with lysosomes to form a phagolysosome.
- Reactive oxygen species (ROS) and other mediators, like nitric oxide (NO), are crucial for degrading and killing ingested microbes.
Cell-Derived Mediators
- Reactive oxygen species (ROS) are produced by neutrophils and macrophages to help destroy pathogens.
- In addition to ROS, nitric oxide (NO) functions as a signaling molecule and effector in inflammatory responses.
- Prostaglandins and leukotrienes derived from arachidonic acid are key mediators in inflammation.
Regulation and Balance
- Antioxidant enzymes are necessary for preventing oxidative damage to healthy tissues during the inflammatory response.
- The immune response includes checks and balances to ensure efficient pathogen clearance while minimizing collateral damage to surrounding tissues.
Functional Role of Nitric Oxide
- Nitric oxide (NO) primarily originates from macrophages and serves multiple roles, including vasodilation and antimicrobial activity.
- NO synthesis is regulated by cytokines and is influenced by the microenvironment during inflammation.
Dendritic Cells and Immune Response
- Dendritic cells have dendrite-like projections, playing a crucial role in the immune system by recognizing microbes and dead cells.
- They capture and present antigens to T cells to enhance immune responses.
Acute Inflammation
- Acute inflammation is a rapid protective response triggered by infections, tissue injury, or chemical toxins.
- Involves vascular reactions leading to increased blood flow and permeability, allowing leukocytes and plasma proteins to enter tissues.
- Critical for delivering immune cells and initiating the repair process.
Tissue-Resident Macrophages
- Macrophages, present in connective tissues and organs, are vital for tissue homeostasis and immune responses.
- They are named variably based on organ location, such as Kupffer cells in the liver and alveolar macrophages in the lungs.
- Origin usually from blood monocytes and can persist long-term in tissues.
Vascular Reactions during Inflammation
- Key changes include blood vessel dilation and increased permeability, resulting in localized redness and swelling (erythema).
- Vascular changes lead to stasis, characterized by slow blood flow and increased concentration of leukocytes, particularly neutrophils, within the first 6 to 24 hours of inflammation.
Role of Leukocytes
- Neutrophils adhere to the endothelium, migrating toward inflamed tissues in response to stimuli.
- Activated leukocytes deliver signals to recruit additional immune cells, orchestrating the inflammatory response.
Pro-inflammatory Mediators
- Prostaglandins and leukotrienes are derived from arachidonic acid and play pivotal roles in mediating inflammation.
- Healthy tissues are typically protected from damage by reactive oxygen species (ROS) through the action of antioxidant enzymes that degrade these harmful agents.
Nitric Oxide in Inflammation
- Nitric oxide (NO) is predominantly produced in macrophages during inflammatory responses.
- Functions in signaling and modulating the vascular responses necessary for effective inflammation and repair.
General Functions of Inflammation
- Inflammation serves to isolate and eliminate infectious agents, clear out necrotic cells, and initiate tissue healing and regeneration.
- Macrophages and other leukocytes are essential for phagocytosing debris and pathogens, supporting tissue regeneration.
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Description
This quiz deals with the effects of acute vessel damage on blood flow, concentration, and inflammation. It also covers the response of small vessels and the increase in blood viscosity.