Persistent colonization of non-lymphoid tissue-resident macrophages by Stenotrophomonas maltophilia.
IL-10
colitis
gut-resident macrophage
intracellular commensal bacteria
symbiotic factor smlt2713
Journal
International immunology
ISSN: 1460-2377
Titre abrégé: Int Immunol
Pays: England
ID NLM: 8916182
Informations de publication
Date de publication:
07 02 2020
07 02 2020
Historique:
received:
24
09
2019
accepted:
17
10
2019
pubmed:
21
10
2019
medline:
2
10
2020
entrez:
21
10
2019
Statut:
ppublish
Résumé
Accumulating evidence has revealed that lymphoid tissue-resident commensal bacteria (e.g. Alcaligenes spp.) survive within dendritic cells. We extended our previous study by investigating microbes that persistently colonize colonic macrophages. 16S rRNA-based metagenome analysis using DNA purified from murine colonic macrophages revealed the presence of Stenotrophomonas maltophilia. The in situ intracellular colonization by S. maltophilia was recapitulated in vitro by using bone marrow-derived macrophages (BMDMs). Co-culture of BMDMs with clinically isolated S. maltophilia led to increased mitochondrial respiration and robust IL-10 production. We further identified a 25-kDa protein encoded by the gene assigned as smlt2713 (recently renamed as SMLT_RS12935) and secreted by S. maltophilia as the factor responsible for enhanced IL-10 production by BMDMs. IL-10 production is critical for maintenance of the symbiotic condition, because intracellular colonization by S. maltophilia was impaired in IL-10-deficient BMDMs, and smlt2713-deficient S. maltophilia failed to persistently colonize IL-10-competent BMDMs. These findings indicate a novel commensal network between colonic macrophages and S. maltophilia that is mediated by IL-10 and smlt2713.
Identifiants
pubmed: 31630178
pii: 5601250
doi: 10.1093/intimm/dxz071
pmc: PMC10689348
doi:
Substances chimiques
IL10 protein, mouse
0
Interleukin-10
130068-27-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
133-141Informations de copyright
© The Author(s) 2019. Published by Oxford University Press on behalf of The Japanese Society for Immunology.
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