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Free Radic Res. 2018 Dec;52(11-12):1328-1335. doi: 10.1080/10715762.2018.1470327. Epub 2018 May 16.

Carbon monoxide ameliorates murine T-cell-dependent colitis through the inhibition of Th17 differentiation.

Author information

1
a Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Science , Kyoto Prefectural University of Medicine , Kyoto , Japan.
2
b Department of Medical Innovation and Translational Medical Science, Graduate School of Medical Science , Kyoto Prefectural University of Medicine , Kyoto , Japan.
3
c Department of Endocrinology and Metabolism, Graduate School of Medical Science , Kyoto Prefectural University of Medicine , Kyoto , Japan.

Abstract

Recent studies have identified carbon monoxide (CO) as a potential therapeutic molecule for the treatment of inflammatory diseases including intestinal inflammation. In the present study, we explored the efficacy and the mechanisms of action of CO-releasing molecule (CORM)-A1 in T-cell transfer induced colitis model in mice. In addition, the impact of CORM-A1 on the T helper (Th) cell differentiation was evaluated using naïve CD4+ T cells isolated from the spleens in Balb/c mice. The results showed that CORM-A1 conferred protection against the development of intestinal inflammation and attenuated Th17 cell differentiation. Hence, the observed immunomodulatory effects of CORM-A1 could be useful for developing novel therapeutic approaches for managing intestinal inflammation through the regulation of Th17 differentiation.

KEYWORDS:

Carbon monoxide; Th17 differentiation; colitis

PMID:
29695203
DOI:
10.1080/10715762.2018.1470327
[Indexed for MEDLINE]

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