BIOM20001 Lecture Notes - Lecture 61: C3B, Respiratory Burst, Gram-Negative Bacteria
Document Summary
Steps of inflammation: recognition --> recruitment --> removal --> regulation --> resolution. Recognition: pamp and damp (injury) recognised by prr. Chemical mediators and direct damage to endothelial cells. Engagement of receptors expressed on leukocyte surfaces by microbial products and mediators of inflammation. Release of substances that destroy extracellular microbes and degrade tissue. Produce cellular mediators to amplify the inflammatory response. Bacterial peptides and inflammatory mediators produced in response to microbes or injury (n-formyl-methionyl peptides which is a modification of a protein found in microorganisms), chemokines, lipid mediators such as prostagladins. Inflammatory mediators (cytokines) produced in response to microbes or injury. Prr, tlr or inflammasome recognises injury/pathogen associated immunostimulant (lps/endotoxin, outer membrane of gram negative bacteria) Igg, breakdown products of complement protein c3, collectins bind to receptors such as fc r1, cr1, cr3, c1q. Bacterial lps activates complement, generating c3b with opsinizing properties. Antibodies bound to antigen activate complement and also act as opsonins.
