Infection with pathogenic bacteria can result in acute or chronic disease, which can be life threatening, especially in young, elderly or other immunocompromised individuals. Humans are also infected with a wide range of commensal bacteria, as part of our normal gut flora, and the immune system must be capable of controlling immune responses against these beneficial bacteria, while at the same time generating effector immune responses against pathogenic micro-organisms. In addition, pathogenic bacteria have evolved strategies for delaying or preventing their elimination by evading or subverting protective immune responses of the host.
Innate immunity to bacteria
The initial inflammatory response to pathogenic bacteria involves the release of cytokines and chemokines and the recruitment of neutrophils, monocytes, dendritic cells (DCs) and lymphocytes to the site of infection. Tissue macrophages and neutrophils quickly phagocytose and attempt to kill the bacteria. Macrophages and DCs are activated through binding of conserved, secreted or cell surface bacterial products to pathogen recognition receptors (PRR). This leads to activation of immune response genes, including those coding for inflammatory cytokines, chemokines and co-stimulatory molecules expressed on the surface of DCs and macrophages, that are involved in antigen presentation (Janeway and Medzhitov, 2002).
Bacteria are phagocytosed by neutrophils and macrophages and this is facilitated through activation of the alternative complement pathway by bacterial cell wall components, resulting in the production of C3b, which together with antibodies help to opsonize the bacteria.