Questions and Answers
Which molecule mediates pain as part of acute inflammation?
What is the role of Toll-like receptors (TLRs) in acute inflammation?
Which enzyme is responsible for the release of arachidonic acid (AA) from the cell membrane?
What is the effect of LTB4 on neutrophils?
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What is the role of Hageman factor (Factor XII) when activated?
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What can lead to clinical manifestations such as delayed umbilical cord separation and recurrent bacterial infections without pus formation?
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Which of the following is a characteristic of 02-independent killing by leukocytes?
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Which cells predominate after neutrophils and peak 2-3 days after inflammation begins?
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What are the outcomes managed by macrophages in the inflammatory process?
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How do macrophages mediate fibrosis in the context of inflammation?
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Study Notes
Inflammatory Mediators and Neutrophil Function
- 5-lipoxygenase produces leukotrienes (LT), which have diverse effects on inflammation.
- LTB4 attracts and activates neutrophils, while LTC4, LTD4, and LTE4 mediate vasoconstriction, bronchospasm, and increased vascular permeability.
- Mast cells, widely distributed throughout connective tissue, are activated by various stimuli, resulting in immediate and delayed inflammatory responses.
- Complement proteins, circulating as inactive precursors, are activated through three pathways, resulting in the production of various proinflammatory mediators.
- Hageman factor (Factor XII) is an inactive proinflammatory protein produced in the liver, which, when activated, affects coagulation, complement, and kinin systems.
- Cardinal signs of inflammation include redness and warmth due to vasodilation, swelling due to fluid leakage, and pain due to sensitization of sensory nerve endings.
- Inflammation is associated with fever, caused by the release of IL-1 and TNF, resulting in increased cyclooxygenase activity.
- Neutrophil arrival and function involve a series of steps, including margination, rolling, adhesion, transmigration, chemotaxis, phagocytosis, and destruction of phagocytosed material.
- Neutrophil rolling and adhesion involve the upregulation of selectins and adhesion molecules on endothelial cells and leukocytes.
- Neutrophil adhesion deficiency, often due to integrin defects, can lead to clinical manifestations such as delayed umbilical cord separation and recurrent bacterial infections without pus formation.
- Phagocytosis is enhanced by opsonins, and defects in phagolysosome formation can lead to conditions such as Chediak-Higashi syndrome.
- Neutrophil destruction of phagocytosed material involves the oxidative burst, which can be defective in conditions like chronic granulomatous disease (CGD) and myeloperoxidase (MPO) deficiency.
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Description
Test your knowledge of inflammatory mediators and neutrophil function with this quiz. Explore the roles of 5-lipoxygenase, leukotrienes, mast cells, complement proteins, and Hageman factor in inflammation. Learn about the cardinal signs of inflammation, the association with fever, and the steps involved in neutrophil arrival and function. Delve into conditions such as neutrophil adhesion deficiency, phagocytosis defects, and neutrophil destruction of phagoc
