Changes

==Innate mechanisms==

==Innate mechanisms==

===Lipopolysaccharide recognition===

====Lipopolysaccharide recognition====

LPS is a component of some Gram-negative bacterial cell walls and its recognition is thought to be an ancient mechanism that evolved before the acquired immune system. When released by bacteria, LPS can bind to soluble CD14, which causes the release of TNF-alpha and IL-1 (both lead to systemic phagocyte activation), or to lipoprotein particles, which neutralize it.

LPS is a component of some Gram-negative bacterial cell walls and its recognition is thought to be an ancient mechanism that evolved before the acquired immune system. When released by bacteria, LPS can bind to soluble CD14, which causes the release of TNF-alpha and IL-1 (both lead to systemic phagocyte activation), or to lipoprotein particles, which neutralize it.

===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 bacteria, e.g. mannose-binding lectin of E. coli.

**Lectins on the phagocyte, e.g. complement receptors such as CR3.

**Lectins on the phagocyte, e.g. complement receptors such as CR3.