Journal
DISEASE MODELS & MECHANISMS
Volume 15, Issue 5, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dmm.049551
Keywords
Drosophila; TOR; Infection; Lipid metabolism; Physiology
Categories
Funding
- Canadian Institutes of Health Research project [PJT 173517]
- Natural Sciences and Engineering Research Council of Canada [RGPIN 2016-04544]
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In enteric infection, TOR signaling pathway is induced in fruit flies, leading to an increase in lipid synthesis gene levels and a reduction in host lipid consumption to promote survival.
When infected by enteric pathogenic bacteria, animals need to initiate local and whole-body defence strategies. Although most attention has focused on the role of innate immune anti-bacterial responses, less is known about how changes in host metabolism contribute to host defence. Using Drosophila as a model system, we identify induction of intestinal target-of-rapamycin (TOR) kinase signalling as a key adaptive metabolic response to enteric infection. We find that enteric infection induces both local and systemic induction of TOR independently of the Immune deficiency (IMD) innate immune pathway, and we see that TOR functions together with IMD signalling to promote infection survival. These protective effects of TOR signalling are associated with remodelling of host lipid metabolism. Thus, we see that TOR is required to limit excessive infection-mediated wasting of host lipid stores by promoting an increase in the levels of gut-and fat body-expressed lipid synthesis genes. Our data support a model in which induction of TOR represents a host tolerance response to counteract infection mediated lipid wasting in order to promote survival.
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