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Glyphosate induces immune dysregulation in honey bees

BACKGROUND: Similar to many other animals, the honey bee Apis mellifera relies on a beneficial gut microbiota for regulation of immune homeostasis. Honey bees exposed to agrochemicals, such as the herbicide glyphosate or antibiotics, usually exhibit dysbiosis and increased susceptibility to bacteria...

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Detalles Bibliográficos
Autores principales: Motta, Erick V. S., Powell, J. Elijah, Moran, Nancy A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8862317/
https://www.ncbi.nlm.nih.gov/pubmed/35193702
http://dx.doi.org/10.1186/s42523-022-00165-0
Descripción
Sumario:BACKGROUND: Similar to many other animals, the honey bee Apis mellifera relies on a beneficial gut microbiota for regulation of immune homeostasis. Honey bees exposed to agrochemicals, such as the herbicide glyphosate or antibiotics, usually exhibit dysbiosis and increased susceptibility to bacterial infection. Considering the relevance of the microbiota–immunity axis for host health, we hypothesized that glyphosate exposure could potentially affect other components of the honey bee physiology, such as the immune system. RESULTS: In this study, we investigated whether glyphosate, besides affecting the gut microbiota, could compromise two components of honey bee innate immunity: the expression of genes encoding antimicrobial peptides (humoral immunity) and the melanization pathway (cellular immunity). We also compared the effects of glyphosate on the bee immune system with those of tylosin, an antibiotic commonly used in beekeeping. We found that both glyphosate and tylosin decreased the expression of some antimicrobial peptides, such as apidaecin, defensin and hymenoptaecin, in exposed honey bees, but only glyphosate was able to inhibit melanization in the bee hemolymph. CONCLUSIONS: Exposure of honey bees to glyphosate or tylosin can reduce the abundance of beneficial gut bacteria and lead to immune dysregulation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42523-022-00165-0.