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Modern clinical Mtb strains leverage the type I IFN pathway for a pro-inflammatory response in the host

Host phagocytes are adept at responding to infections by innate immune mechanisms and metabolic alterations designed to restrict the invading pathogen. However, this very plasticity of the response provides an ideal platform for pathogen mediated manipulation. Clinical lineages of Mycobacterium tuberculosis have evolved distinct and numerous ways of achieving optimal infection. We demonstrate an early, active and prominent induction of the macrophage type I IFN response by the modern lineages (L3 and L4) in contrast to the protracted and diminished capacity of the ancient Mtb lineage L1. We also establish a unique link between this augmented IFN response and increased expression of the CH25H, a pro-inflammatory signaling molecule that regulates the early and enhanced pro-inflammatory response (IL6) in macrophages infected with modern Mtb strains. We reveal a strong correlation between the localization of modern Mtb to acidified phagosomes and the ability to induce type I IFN in macrophages highlighting yet another unique ability of Mtb to manipulate host cell physiology to foster a pro-inflammatory response from host phagocytes.