Immune Evasion by Extracellular Bacteria

The virulence of extracellular bacteria has been linked to a number of mechanisms that resist innate immunity (Table 15-2), including antiphagocytic mechanisms and inhibition of complement or inactivation of complement products. Bacteria with polysaccharide-rich capsules resist phagocytosis and are therefore much more virulent than homologous strains lacking a capsule. The capsules of many pathogenic gram-positive and gram-negative bacteria contain sialic acid residues that inhibit complement activation by the alternative pathway.

A mechanism used by bacteria to evade humoral immunity is genetic variation of surface antigens. Some surface antigens of bacteria such as gonococci and Escherichia coli are contained in their pili, which are the structures responsible for bacterial adhesion to host cells. The major antigen of the pili is a protein called pilin. The pilin genes of gonococci undergo extensive gene conversion, because of which the progeny of one organism can produce up to 106 antigenically distinct pilin molecules. This ability to alter antigens helps the bacteria evade attack by pilin-specific antibodies, although its principal significance for the bacteria may be to select for pili that are more adherent to host cells so that the bacteria are more virulent. In other bacteria, such as Haemophilus influenzae, changes in the production of glycosidases lead to chemical alterations in surface LPS and other polysac-charides, which enable the bacteria to evade humoral immune responses against these antigens.

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