Abstract
Male and female animals exhibit differences in infection outcomes. One possible source of sexually dimorphic immunity is the sex-specific costs of immune activity or pathology, but little is known about the independent effects of immune- versus microbe-induced pathology and whether these may differ for the sexes. Here, by measuring metabolic and physiological outputs in Drosophila melanogaster with wild-type and mutant immune responses, we test whether the sexes are differentially impacted by these various sources of pathology and identify a critical regulator of this difference. We find that the sexes exhibit differential immune activity but similar bacteria-derived metabolic pathology. We show that female-specific immune-inducible expression of PGRP-LB, a negative regulator of the immune deficiency (IMD) pathway, enables females to reduce immune activity in response to reductions in bacterial numbers. In the absence of PGRP-LB, females are more resistant to infection, confirming the functional importance of this regulation and suggesting that female-biased immune restriction comes at a cost.
Highlights
Male and female animals exhibit differences in infection outcomes
We show that females reduce the cost of immune activity via strict regulation of the immune deficiency (IMD) pathway and that this comes at the cost of bacterial clearance
To determine whether male and female flies exhibited a difference in their ability to defend against nonpathogenic gram-negative bacterial infection, we first measured survival and bacterial numbers after infection with E. coli of w1118 flies
Summary
Male and female animals exhibit differences in infection outcomes. One possible source of sexually dimorphic immunity is the sexspecific costs of immune activity or pathology, but little is known about the independent effects of immune- versus microbe-induced pathology and whether these may differ for the sexes. The survival and continued health of the host will be the product of a complex interaction of host and pathogen genotype as well as other factors It is unclear whether the welldocumented effects of host sex on infection outcome in general primarily originate in changes in resistance to the infectious agent or in tolerance of direct or indirect pathology. To distinguish these effects, we used the fruit fly Drosophila melanogaster and consider the response of w1118 control and immunocompromised flies to infection with the bacterium Escherichia coli. We show that females reduce the cost of immune activity via strict regulation of the immune deficiency (IMD) pathway and that this comes at the cost of bacterial clearance
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