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Mycobacterium tuberculosis activates the DNA-dependent cytosolic surveillance pathway within macrophages.

Abstract：

:Cytosolic bacterial pathogens activate the cytosolic surveillance pathway (CSP) and induce innate immune responses, but how the host detects vacuolar pathogens like Mycobacterium tuberculosis is poorly understood. We show that M. tuberculosis also initiates the CSP upon macrophage infection via limited perforation of the phagosome membrane mediated by the ESX-1 secretion system. Although the bacterium remains within the phagosome, this permeabilization results in phagosomal and cytoplasmic mixing and allows extracellular mycobacterial DNA to access host cytosolic receptors, thus blurring the distinction between "vacuolar" and "cytosolic" pathogens. Activation of cytosolic receptors induces signaling through the Sting/Tbk1/Irf3 axis, resulting in IFN-β production. Surprisingly, Irf3(-/-) mice, which cannot respond to cytosolic DNA, are resistant to long-term M. tuberculosis infection, suggesting that the CSP promotes M. tuberculosis infection. Thus, cytosolic sensing of mycobacterial DNA plays a key role in M. tuberculosis pathogenesis and likely contributes to the high type I IFN signature in tuberculosis.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Manzanillo PS,Shiloh MU,Portnoy DA,Cox JS

doi

10.1016/j.chom.2012.03.007

subject

Has Abstract

pub_date

2012-05-17 00:00:00

pages

469-80

issue

5

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(12)00125-4

journal_volume

11

pub_type

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