Anti-inflammatory Bifidobacterium strains prevent dextran sodium sulfate induced colitis and associated gut microbial dysbiosis in mice
Crohn’s and ulcerative colitis are common inflammatory conditions associated with Inflammatory bowel disease. Owing to the importance of diet based approaches for the prevention of inflammatory gut conditions, the present study was aimed to screen the human isolates of Bifidobacterium strains based...
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Veröffentlicht in: | Scientific reports 2020-10, Vol.10 (1), p.18597, Article 18597 |
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Sprache: | eng |
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Zusammenfassung: | Crohn’s and ulcerative colitis are common inflammatory conditions associated with Inflammatory bowel disease. Owing to the importance of diet based approaches for the prevention of inflammatory gut conditions, the present study was aimed to screen the human isolates of
Bifidobacterium
strains based on their ability to reduce LPS-induced inflammation in murine macrophage (RAW 264.7) cells and to evaluate prioritized strains for their preventive efficacy against ulcerative colitis in mice. Twelve out of 25 isolated strains reduced the production of LPS-induced nitric oxide and inflammatory cytokines. Furthermore, three strains,
B. longum
Bif10
, B. breve
Bif11
, and B. longum
Bif16 conferred protection against dextran sodium sulfate induced colitis in mice. The three strains prevented shortening of colon, spleen weight, percentage body weight change and disease activity index relative to colitis mice. Lower levels of Lipocalin-2, TNF-α, IL-1β and IL-6 and improved SCFA levels were observed in
Bifidobacterium
supplemented mice relative to DSS counterparts. Bacterial composition of
B. longum
Bif10 and
B. breve
Bif11 fed mice was partly similar to the normal mice, while DSS and
B. longum
Bif16 supplemented mice showed deleterious alterations. At the genus level,
Bifidobacterium
supplementation inhibited the abundances of pathobionts such as
Haemophilus
,
Klebsiella
and
Lachnospira
there by conferring protection. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-020-75702-5 |