Perspectives on host adaptation in response to Mycobacterium tuberculosis: modulation of inflammation.

摘要: Tuberculosis (TB) is the outcome of an insidious, protracted infection with Mycobacterium tuberculosis (Mtb). It primarily affects lung and characterized by extensive focal inflammation development granulomas. TB therefore a chronic inflammatory condition in which regulatory pro-inflammatory processes, occurring mutually or stage-wise, contribute to disease establishment progression. Most host components involved inflammation, including cytokines (interferons, interleukin (IL)-1, IL-10, tumour necrosis factor) cells (neutrophils, macrophages, T cells, type 1 helper lymphocytes, pneumocytes), exhibit dual features: they foster repress local events. As consequence, selected mediators can limit facilitate depending on their temporal tissue dynamics. Distinct defence elements not only genesis granulomas, but also progression cavitation implicitly transmission. Altogether, these pathogenesis traits highlight that evolutionary success Mtb relies its capacity modulate own benefit. Both pro- anti-inflammatory events are exploited as bacterial evasion strategies defence.