1,473
edits
Changes
no edit summary
==Overview==
==Overview==
Some bacteria, particularly those with an outer lipid bilayer (i.e. Gram-negative), are susceptible to [[Complement]] activated via the alternative pathway (the lytic complex: C5b-9). The release of C3a and C5a lead to histamine release, and attracts and activates [[Neutrophils|neutrophils]]. Components of C3 aid opsonisation of the bacteria.
Some bacteria, particularly those with an outer lipid bilayer (i.e. Gram-negative), are susceptible to [[Complement]] activated via the alternative pathway (the lytic complex: C5b-9). The release of C3a and C5a lead to histamine release, and attracts and activates [[Neutrophils|neutrophils]]. Components of C3 aid opsonisation of the bacteria.
==Phagocytosis==
===Phagocytosis===
Most bacteria are killed this way. [[Complement products]], bacterial components (e.g. f-Met-Leu-Phe) and locally released cytokines are chemotactic for phagocytes. The binding of the phagocyte can be mediated by the following;
Most bacteria are killed this way. [[Complement products]], bacterial components (e.g. f-Met-Leu-Phe) and locally released cytokines are chemotactic for phagocytes. The binding of the phagocyte can be mediated by the following:
**Lectins on the bacteria, e.g. mannose-binding lectin of E. coli.
**Lectins on the phagocyte, e.g. complement receptors such as CR3.
**[[Complement]] deposited on the organism, both classic and alternative pathways.
**Fc receptors on phagocyte, bind to the antibody on bacteria.
The activation of [[Macrophages|macrophages]] occurs after exposure to microbial products or T cell-derived lymphokines. Lymphokines released during T-cell activation are often required for full activation, such as IFN-γ.
The activation of [[Macrophages|macrophages]] occurs after exposure to microbial products or T cell-derived lymphokines. Lymphokines released during T-cell activation are often required for full activation, such as IFN-γ.