Role of type I cytokines in host defense against Mycobacterium avium infection

Mycobacterium avium is a human pathogen that causes infection in immunocompetent as well as immunocompromised patients. Infection is acquired both by the respiratory and gastrointestinal routes, and bacterial invasion of mucosal epithelial cells is characteristic. M avium crosses the mucosal barrier without triggering substantial inflammatory response. Once in the intestinal submucosa or in the alveolar space M. avium infects macrophages. Intracellular bacteria block the production of cytokines involved in the host response against the infection, such as TNF-alpha and IL-12, and suppress antigen presentation by the macrophage. Innate response against the infection is effective to certain extent but the ability of the bacterium to remain "silent" for a period of time prevents neutrophil and NK cells from effectively controlling the establishing of the infection. CD4+ T cells as well as CD8+ T cells are activated, although only CD4+ T cells appear to be effective in inducing anti-M avium activity in macrophages. M avium-specific CD8+ T cells undergo apoptosis early in the infection. Therefore, the immune mechanisms of the host and bacterial strategies for survival are complex and fascinating.