Abstract
Many have argued that we may be able to extend life and improve human health through hormesis, the beneficial effects of low-level toxins and other stressors. But, studies of hormesis in model systems have not yet established whether stress-induced benefits are cost free, artifacts of inbreeding, or come with deleterious side effects. Here, we provide evidence that hormesis results in trade-offs with immunity. We find that a single topical dose of dead spores of the entomopathogenic fungus, Metarhizium robertsii, increases the longevity of the fruit fly, Drosophila melanogaster, without significant decreases in fecundity. We find that hormetic benefits of pathogen challenge are greater in lines that lack key components of antifungal immunity (Dif and Turandot M). And, in outbred fly lines, we find that topical pathogen challenge enhances both survival and fecundity, but reduces ability to fight off live infections. The results provide evidence that hormesis is manifested by stress-induced trade-offs with immunity, not cost-free benefits or artifacts of inbreeding. Our findings illuminate mechanisms underlying pathogen-induced life-history trade-offs, and indicate that reduced immune function may be an ironic side effect of the “elixirs of life.”
Highlights
We find that a single topical dose of dead spores of the entomopathogenic fungus, Metarhizium robertsii, increases the longevity of the fruit fly, Drosophila melanogaster, without significant decreases in fecundity
The results provide evidence that hormesis is manifested by stress-induced trade-offs with immunity, not cost-free benefits or artifacts of inbreeding
We investigated Dif because it is a key component of the Toll pathway, which confers antifungal immunity and is a putative regulator of hormesis (Le Bourg et al 2012); Turandot M because it is upregulated in response to infection and provides protection against sexually fungal transmitted infections in flies (Ekengren and Hultmark 2001; Brun et al 2006; Zhong et al 2013); Hsp83 as a positive control because previous work has established that stress-associated molecular chaperones are essential for hormesis (Tatar et al 1997; Qin et al 2005); and Turandot C because it is upregulated in response to many different types of stress and we had previously established that there was no evidence that it confers immunity to topical fungal infection (Zhong et al 2013)
Summary
General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. These are important questions to resolve because they relate to how animals fight off infections and whether we can use stress treatments to improve health, and because they provide a crucial test of the evolutionary principle that life-history optimization is constrained We address these questions using the fruit fly, Drosophila melanogaster as host for the insect-generalist entomopathogic fungus, Metarhizium robertsii (for further details, see Gao et al 2011; Zhong et al 2013). This system has several features that make it suitable for studies of pathogen-induced fitness trade-offs and the age-specific genetic effects, which underlie hormesis: topical application of dead Metarhizium spores is known to stimulate immune responses in insects (Xia et al 2001). We tested two wild-type lines, Oregon-R, a standard outbred laboratory-adapted line maintained in two-week culture (Milkman 1966), and Dahomey, another standard laboratory-adapted line maintained in large populations under age-independent culture (Chapman and Partridge 1996)
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