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Abstract
The gastrointestinal tract harbors a diverse microbiota that has coevolved with mammalian
hosts. Though most associations are symbiotic or commensal, some resident bacteria
(termed pathobionts) have the potential to cause disease. Bacterial type VI secretion
systems (T6SSs) are one mechanism for forging host-microbial interactions. Here we
reveal a protective role for the T6SS of Helicobacter hepaticus, a Gram-negative bacterium
of the intestinal microbiota. H. hepaticus mutants with a defective T6SS display increased
numbers within intestinal epithelial cells (IECs) and during intestinal colonization.
Remarkably, the T6SS directs an anti-inflammatory gene expression profile in IECs,
and CD4+ T cells from mice colonized with T6SS mutants produce increased interleukin-17
in response to IECs presenting H. hepaticus antigens. Thus, the H. hepaticus T6SS
limits colonization and intestinal inflammation, promoting a balanced relationship
with the host. We propose that disruption of such balances contributes to human disorders
such as inflammatory bowel disease and colon cancer.
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