2021
DOI: 10.1073/pnas.2026554118
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Disparate regulation of IMD signaling drives sex differences in infection pathology in Drosophila melanogaster

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 sou… Show more

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Cited by 30 publications
(43 citation statements)
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“…In line with this, several of the treatments employed in this study, e.g., L. monocytogenes or E. coli infections and genetic activation of the Toll pathway in the fat body, have been shown to interfere with the insulin signalling pathway and subsequently decrease nutrient storage or growth [45,67,68]. Moreover, infections with L. monocytogenes and E. coli, as well as numerous pathogens, cause systemic changes in metabolic signalling [32,45,68,69]. Yet, despite the marked metabolic switch triggered during systemic infections, male and female flies retain their pre-copulatory behaviours.…”
Section: Discussionsupporting
confidence: 60%
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“…In line with this, several of the treatments employed in this study, e.g., L. monocytogenes or E. coli infections and genetic activation of the Toll pathway in the fat body, have been shown to interfere with the insulin signalling pathway and subsequently decrease nutrient storage or growth [45,67,68]. Moreover, infections with L. monocytogenes and E. coli, as well as numerous pathogens, cause systemic changes in metabolic signalling [32,45,68,69]. Yet, despite the marked metabolic switch triggered during systemic infections, male and female flies retain their pre-copulatory behaviours.…”
Section: Discussionsupporting
confidence: 60%
“…Activation of immune responses by exposure to pathogens limits resource utilisation towards other important biological processes. In line with this, several of the treatments employed in this study, e.g., L. monocytogenes or E. coli infections and genetic activation of the Toll pathway in the fat body, have been shown to interfere with the insulin signalling pathway and subsequently decrease nutrient storage or growth [45,67,68]. Moreover, infections with L. monocytogenes and E. coli, as well as numerous pathogens, cause systemic changes in metabolic signalling [32,45,68,69].…”
Section: Discussionsupporting
confidence: 57%
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“…For example, female flies lacking the negative epigenetic regulator G9a, were found to be more tolerant than males during viral infections (Gupta and Vale 2017). Similar examples also exist from other innate immune pathways where, disrupting the negative regulator of IMD, PGRP-LB (peptidoglycan receptor-LB), affected survival to a greater extent in females following E. coli infection, suggesting the sex-specific role of some of these regulators (Vincent and Dionne 2021). The combination of these observations might explain why flies lacking Socs36E showed sex differences in disease tolerance, particularly in light of the crosstalk between Jak/Stat and IMD pathways (Kemp et al 2013;Bang 2019;Dostert et al 2005).…”
Section: During Systemic Bacterial Infection Loss Of Jak-stat Signalling Leads To Sex Differences In Disease Tolerance Phenotypesmentioning
confidence: 74%