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Autophagy restricts Mycobacterium tuberculosis during acute infection in mice
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Journal Article
Autophagy restricts Mycobacterium tuberculosis during acute infection in mice
2023
Overview
Whether or not autophagy has a role in defence against
Mycobacterium tuberculosis
infection remains unresolved. Previously, conditional knockdown of the core autophagy component ATG5 in myeloid cells was reported to confer extreme susceptibility to
M. tuberculosis
in mice, whereas depletion of other autophagy factors had no effect on infection. We show that doubling
cre
gene dosage to more robustly deplete ATG16L1 or ATG7 resulted in increased
M. tuberculosis
growth and host susceptibility in mice, although ATG5
-
depleted mice are more sensitive than ATG16L1- or ATG7-depleted mice. We imaged individual macrophages infected with
M. tuberculosis
and identified a shift from apoptosis to rapid necrosis in autophagy-depleted cells. This effect was dependent on phagosome permeabilization by
M. tuberculosis
. We monitored infected cells by electron microscopy, showing that autophagy protects the host macrophage by partially reducing mycobacterial access to the cytosol. We conclude that autophagy has an important role in defence against
M. tuberculosis
in mammals.
Autophagy-mediated control of
Mycobacterium tuberculosis
acute infection in mice is uncovered by more complete knockouts in autophagy pathway genes.
