Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of interleukin-22.
Animals
Anti-Bacterial Agents
/ adverse effects
Disease Susceptibility
Female
Gastrointestinal Microbiome
/ drug effects
Gene Expression Profiling
Interleukins
/ metabolism
Intestinal Mucosa
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Real-Time Polymerase Chain Reaction
Rotavirus
/ physiology
Rotavirus Infections
/ etiology
Interleukin-22
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2021
2021
Historique:
received:
11
02
2021
accepted:
13
05
2021
entrez:
12
8
2021
pubmed:
13
8
2021
medline:
23
11
2021
Statut:
epublish
Résumé
The commensal microbiota regulates susceptibility to enteric pathogens by fine-tuning mucosal innate immune responses, but how susceptibility to enteric viruses is shaped by the microbiota remains incompletely understood. Past reports have indicated that commensal bacteria may either promote or repress rotavirus replication in the small intestine of mice. We now report that rotavirus replicated more efficiently in the intestines of germ-free and antibiotic-treated mice compared to animals with an unmodified microbiota. Antibiotic treatment also facilitated rotavirus replication in type I and type III interferon (IFN) receptor-deficient mice, revealing IFN-independent proviral effects. Expression of interleukin-22 (IL-22) was strongly diminished in the intestine of antibiotic-treated mice. Treatment with exogenous IL-22 blocked rotavirus replication in microbiota-depleted wild-type and Stat1-/- mice, demonstrating that the antiviral effect of IL-22 in animals with altered microbiome is not dependent on IFN signaling. In antibiotic-treated animals, IL-22-induced a specific set of genes including Fut2, encoding fucosyl-transferase 2 that participates in the biosynthesis of fucosylated glycans which can mediate rotavirus binding. Interestingly, IL-22 also blocked rotavirus replication in antibiotic-treated Fut2-/- mice. Furthermore, IL-22 inhibited rotavirus replication in antibiotic-treated mice lacking key molecules of the necroptosis or pyroptosis pathways of programmed cell death. Taken together, our results demonstrate that IL-22 determines rotavirus susceptibility of antibiotic-treated mice, yet the IL-22-induced effector molecules conferring rotavirus resistance remain elusive.
Identifiants
pubmed: 34383769
doi: 10.1371/journal.pone.0247738
pii: PONE-D-21-04729
pmc: PMC8360596
doi:
Substances chimiques
Anti-Bacterial Agents
0
Interleukins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0247738Subventions
Organisme : NIH HHS
ID : R01 OD024917
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI141716
Pays : United States
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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