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TIPE-2 ameliorates inflammatory bowel disease in mice via inhibiting STAT3 and NF-kB activation

Shouzhi Zhou1, Zhao Yang2, Jiaxin Liu2

  • 1Department of Proctology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.

Immunology Letters
|February 27, 2023
PubMed

TIPE-2 has been identified as a negative regulator of both innate and adaptive immunity and is involved in several inflammatory diseases. However, the immune inhibition mechanism of TIPE-2 involved in inflammatory bowel disease has not been well studied. Therefore, the aim of this study was to investigate whether TIPE-2 improved experimental colitis by reducing high levels of inflammation in the intestine. Lentivirus encoding TIPE-2 was administered to mice by intrarectal injection after colitis induction. Histological analysis was used to analyze sections of the intestine. Protein expression induced by STAT3 and NF-κB signaling was analyzed by western blot. We found that TIPE-2 reduced the colitis activity index score and the histological score of the intestine. TIPE-2 also decreased inflammatory cytokine levels in the intestine. Additionally, TIPE-2 inhibited STAT3 and NF-kB activation. These results suggested that TIPE-2 might attenuate inflammation of colitis via inhibiting of STAT3 and NF-kB activation.

Keywords:
Inflammatory bowel diseaseNF-kBSTAT3TIPE-2

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