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

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