Journal
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
Volume 378, Issue 1882, Pages -Publisher
ROYAL SOC
DOI: 10.1098/rstb.2022.0121
Keywords
stress; corticosterone; ecoimmunology; ranavirus; amphibian; microbiome
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This study investigated how increasing salinization and nutritional algae influenced gut bacterial assembly, host physiology, and responses to ranavirus exposure in larval wood frogs. The results showed that elevating salinity and supplementing with algae increased larval growth and ranavirus loads. However, larvae given algae did not exhibit stress responses observed in larvae fed a basic diet, indicating a potentially adaptive stress response reversal. Algal supplementation also reduced gut bacterial diversity, with higher relative abundances of Firmicutes associated with host metabolism and endocrine function regulation.
Greater knowledge of how host-microbiome interactions vary with anthropogenic environmental change and influence pathogenic infections is needed to better understand stress-mediated disease outcomes. We investigated how increasing salinization in freshwaters (e.g. due to road de-icing salt runoff) and associated increases in growth of nutritional algae influenced gut bacterial assembly, host physiology and responses to ranavirus exposure in larval wood frogs (Rana sylvatica). Elevating salinity and supplementing a basic larval diet with algae increased larval growth and also increased ranavirus loads. However, larvae given algae did not exhibit elevated kidney corticosterone levels, accelerated development or weight loss post-infection, whereas larvae fed a basic diet did. Thus, algal supplementation reversed a potentially maladaptive stress response to infection observed in prior studies in this system. Algae supplementation also reduced gut bacterial diversity. Notably, we observed higher relative abundances of Firmicutes in treatments with algae-a pattern consistent with increased growth and fat deposition in mammals-that may contribute to the diminished stress responses to infection via regulation of host metabolism and endocrine function. Our study informs mechanistic hypotheses about the role of microbiome mediation of host responses to infection that can be tested in future experiments in this host-pathogen system.This article is part of the theme issue 'Amphibian immunity: stress, disease and ecoimmunology'.
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