Final answer:
C3a and C5a are anaphylatoxins produced during complement activation that significantly contribute to the inflammatory response by increasing vascular permeability, recruiting phagocytes such as neutrophils and macrophages, and amplifying inflammation through additional mediators.
Step-by-step explanation:
During complement activation, the anaphylatoxins C3a and C5a play crucial roles in mediating the physiological response of inflammation. Complement activation occurs via two main pathways: the classical and alternate pathways. Both result in the cleavage of the C3 protein, leading to the formation of C3a and C3b fragments. While C3b opsonizes pathogens for phagocytosis, C3a diffuses away from the site of activation, attracting phagocytes to the site of infection. C5a, derived from the cleavage of C5, serves a similar function.
The inflammatory response is characterized by signs of heat, redness, pain, and swelling, which can occur due to infection or tissue injury. C3a and C5a enhance this response by increasing vascular permeability, allowing for an influx of immune cells and fluid into the tissue, leading to swelling and promoting the arrival of phagocytes, including neutrophils and macrophages, at the site of inflammation. These cells are critical for the eradication of pathogens and initiation of the healing process.
C3a and C5a also act on various cell types to release additional inflammatory mediators, further amplifying the inflammatory response. These actions help in walling off the infection, preventing its spread, and preparing the tissue for repair. However, excessive activation can lead to tissue damage, as seen in hypersensitivity reactions such as type III hypersensitivity. Here, immune complexes activate the complement system, contributing to inflammation and tissue injury.