Inflammation in tuberculosis: interactions, imbalances and interventions

Abstract

Inflammation is critical for tuberculosis (TB) pathogenesis. The nonresolving aspect of inflammation in TB is caused by sophisticated intracellular survival strategies of tubercle bacilli. TB is a continuum comprising a spectrum of lesions as a consequence of complex regulation of inflammation. Proinflammatory cytokines, including interferons, tumor necrosis factor and interleukin 1 along with microRNAs and eicosanoids form an interactive network during TB. Cross-regulation between proinflammatory mediators strongly impacts on infected cell death patterns. These processes, in concert with local concentrations of proteases, such as cathepsins, serpins and matrix-metalloproteinases, affect tissue integrity, shape the architecture of granulomas and modulate tissue repair. With inflammation networks being uncovered in TB, the relevance of several pathways for novel interventions becomes clearer.