IL-33 ameliorates experimental colitis involving regulation of autophagy of macrophages in mice
Autor: | Chang Qi, Lifeng Shi, Min Fang, Zhongyan Wang, Shuyao Hua |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
TNBS-induced experimental colitis lcsh:Biotechnology medicine.medical_treatment Intraperitoneal injection General Biochemistry Genetics and Molecular Biology lcsh:Biochemistry 03 medical and health sciences 0302 clinical medicine In vivo lcsh:TP248.13-248.65 medicine Autophagy lcsh:QD415-436 TLR4 Colitis lcsh:QH301-705.5 business.industry Research Macrophages medicine.disease Interleukin 33 030104 developmental biology medicine.anatomical_structure lcsh:Biology (General) 030220 oncology & carcinogenesis Cancer research IL-33 Bone marrow Stem cell business |
Zdroj: | Cell & Bioscience Cell & Bioscience, Vol 9, Iss 1, Pp 1-9 (2019) |
ISSN: | 2045-3701 |
Popis: | Background Previously, we have demonstrated that IL-33 administration protecting TNBS-induced experimental colitis is associated with facilitation of Th2/Tregs responses in mice. However, whether IL-33 regulates autophagy to ameliorate experimental colitis is unclear. Results IL-33 administration (2 μg/day, intraperitoneal injection), while facilitating Th2/Tregs responses, also enhances the autophagy in mice with TNBS-induced colitis as well as macrophages. In the meantime, we observed that inhibition of the autophagy with 3-methyladenine (3-MA) (24 mg/kg, intraperitoneal injection) in mice exacerbates TNBS-induced experimental colitis. On the contrary, administration of rapamycin (2 mg/kg,intragastric administration), an autophagy-enhancer, alleviates the colitis in mice. In vivo, Immunofluorescence analysis revealed that TNBS combined with IL-33 enhanced the autophagy of macrophages in the inflammatory gut tissue. In vitro, treatment with IL-33 promoted the autophagy of macrophages generated from bone marrow cells in dose-dependant manner. Furthermore, the effect of autophagy-enhancement by IL-33 is TLR4 signaling pathway dependant. Our notion was further confirmed by IL-33-deficient bone marrow-derived macrophages cells. Conclusions IL-33 regulates the autophagy is a new immunoregulatory property on TNBS-induced experimental colitis in mice. |
Databáze: | OpenAIRE |
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