16 Questions
Explain the function of the complement system in immunity.
The complement system functions in both innate and adaptive immunity for defense against microbial pathogens. Complement proteins are present in inactive forms in the plasma, and many of them are activated to become proteolytic enzymes that degrade other complement proteins, thus forming an enzymatic cascade capable of tremendous amplification.
What are the three pathways for the cleavage of C3 in complement activation?
The three pathways for the cleavage of C3 in complement activation are the classical pathway, the alternative pathway, and the lectin pathway.
Describe the formation of the C3 convertase and its function.
Complement activation leads to the formation of an enzyme called the C3 convertase, which splits C3 into two functionally distinct fragments, C3a and C3b. C3a is released, and C3b becomes covalently attached to the cell or molecule where the complement is being activated.
What is the ultimate result of complement activation and how does it occur?
The ultimate result of complement activation is the formation of the membrane attack complex (MAC, composed of multiple C9 molecules). This occurs when C5b binds the late components (C6–C9), culminating in the formation of the MAC.
Inflammation is controlled by which regulatory proteins?
C1 inhibitor, decay accelerating factor (DAF), CD59, and others
What are the key functions of C5a, C4a, and C3a in inflammation?
They stimulate histamine release, increase vascular permeability, and cause vasodilation
What is the role of C5a in inflammation?
C5a is a chemotactic agent for various types of white blood cells and activates the lipoxygenase pathway of arachidonic acid metabolism
How do C3b and iC3b contribute to inflammation?
They act as opsonins and promote phagocytosis by neutrophils and macrophages
What is the function of the membrane attack complex (MAC) in inflammation?
The deposition of MAC on cells results in their osmotic death (lysis), which is important for killing microbes
What are some other mediators of inflammation mentioned in the text?
Platelet-Activating Factor (PAF), Coagulation products, and Kinins
What characterizes acute inflammatory reactions?
Dilation of small blood vessels and accumulation of leukocytes and fluid in the extravascular tissue
What is the defining feature of serous inflammation?
Exudation of cell-poor fluid into spaces created by injury, not infected by destructive organisms
What is the main feature of fibrinous inflammation?
The formation and deposition of fibrin in the extracellular space, which may lead to scarring
What does purulent (suppurative) inflammation lead to the production of?
Pus, consisting of neutrophils, necrotic cell debris, and edema fluid
What are ulcers in the context of inflammation?
Local defects or excavations of the surface of an organ or tissue, produced by the sloughing of inflamed necrotic tissue
What are the outcomes of acute inflammation?
Complete resolution, healing by connective tissue replacement (scarring), and progression to chronic inflammation when the acute response cannot be resolved
Study Notes
Inflammation and its Mediators: Key Points
- C5a, C4a, and C3a are cleavage products of complement components that stimulate histamine release, increase vascular permeability, and cause vasodilation.
- C5a is a chemotactic agent for various types of white blood cells and activates the lipoxygenase pathway of arachidonic acid metabolism.
- C3b and iC3b act as opsonins and promote phagocytosis by neutrophils and macrophages.
- The deposition of the membrane attack complex (MAC) on cells results in their osmotic death (lysis), important for killing microbes.
- Complement activation is controlled by regulatory proteins such as C1 inhibitor, decay accelerating factor (DAF), CD59, and others.
- Other mediators of inflammation include Platelet-Activating Factor (PAF), Coagulation products, and Kinins.
- Acute inflammatory reactions are characterized by dilation of small blood vessels and accumulation of leukocytes and fluid in the extravascular tissue.
- Serous Inflammation involves exudation of cell-poor fluid into spaces created by injury, not infected by destructive organisms.
- Fibrinous Inflammation involves the formation and deposition of fibrin in the extracellular space, which may lead to scarring.
- Purulent (Suppurative) Inflammation leads to the production of pus, consisting of neutrophils, necrotic cell debris, and edema fluid.
- Ulcers are local defects or excavations of the surface of an organ or tissue, produced by the sloughing of inflamed necrotic tissue.
- Outcomes of acute inflammation include complete resolution, healing by connective tissue replacement (scarring), and progression to chronic inflammation when the acute response cannot be resolved.
Test your knowledge of inflammation and its mediators with this quiz. Explore key points about complement components, opsonins, membrane attack complex, and other inflammatory mediators. Learn about acute inflammatory reactions, serous inflammation, fibrinous inflammation, purulent inflammation, and outcomes of acute inflammation.
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