pH-mediated inhibition of a bumble bee parasite by an intestinal symbiont.
Cell-free supernatant
Firmicutes
Trypanosomatidae
competition
flagellates
lactic acid bacteria
microbiome
pH-dependent interactions
parasite strain variation
pollinator decline
Journal
Parasitology
ISSN: 1469-8161
Titre abrégé: Parasitology
Pays: England
ID NLM: 0401121
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
pubmed:
25
9
2018
medline:
4
3
2020
entrez:
25
9
2018
Statut:
ppublish
Résumé
Gut symbionts can augment resistance to pathogens by stimulating host-immune responses, competing for space and nutrients, or producing antimicrobial metabolites. Gut microbiota of social bees, which pollinate many crops and wildflowers, protect hosts against diverse infections and might counteract pathogen-related bee declines. Bumble bee gut microbiota, and specifically abundance of Lactobacillus 'Firm-5' bacteria, can enhance resistance to the trypanosomatid parasite Crithidia bombi. However, the mechanism underlying this effect remains unknown. We hypothesized that the Firm-5 bacterium Lactobacillus bombicola, which produces lactic acid, inhibits C. bombi via pH-mediated effects. Consistent with our hypothesis, L. bombicola spent medium inhibited C. bombi growth via reduction in pH that was both necessary and sufficient for inhibition. Inhibition of all parasite strains occurred within the pH range documented in honey bees, though sensitivity to acidity varied among strains. Spent medium was slightly more potent than HCl, d- and l-lactic acids for a given pH, suggesting that other metabolites also contribute to inhibition. Results implicate symbiont-mediated reduction in gut pH as a key determinant of trypanosomatid infection in bees. Future investigation into in vivo effects of gut microbiota on pH and infection intensity would test the relevance of these findings for bees threatened by trypanosomatids.
Identifiants
pubmed: 30246672
pii: S0031182018001555
doi: 10.1017/S0031182018001555
pmc: PMC6740235
mid: NIHMS1047506
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
380-388Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM122062
Pays : United States
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