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Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis.
World J Gastroenterol. 2017 Feb 14; 23(6):999-1009.WJ

Abstract

AIM

To investigate potential effects of poly I:C on mucosal injury and epithelial barrier disruption in dextran sulfate sodium (DSS)-induced acute colitis.

METHODS

Thirty C57BL/6 mice were given either regular drinking water (control group) or 2% (w/v) DSS drinking water (model and poly I:C groups) ad libitum for 7 d. Poly I:C was administrated subcutaneously (20 μg/mouse) 2 h prior to DSS induction in mice of the poly I:C group. Severity of colitis was evaluated by disease activity index, body weight, colon length, histology and myeloperoxidase (MPO) activity, as well as the production of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin 17 (IL-17) and interferon-γ (IFN-γ). Intestinal permeability was analyzed by the fluorescein isothiocyanate labeled-dextran (FITC-D) method. Ultrastructural features of the colon tissue were observed under electron microscopy. Expressions of tight junction (TJ) proteins, including zo-1, occludin and claudin-1, were measured by immunohistochemistry/immunofluorescence, Western blot and real-time quantitative polymerase chain reaction (RT-qPCR).

RESULTS

DSS caused significant damage to the colon tissue in the model group. Administration of poly I:C dramatically protected against DSS-induced colitis, as demonstrated by less body weight loss, lower disease activity index score, longer colon length, colonic MPO activity, and improved macroscopic and histological scores. It also ameliorated DSS-induced ultrastructural changes of the colon epithelium, as observed under scanning electron microscopy, as well as FITC-D permeability. The mRNA and protein expressions of TJ protein, zo-1, occludin and claudin-1 were also found to be significantly enhanced in the poly I:C group, as determined by immunohistochemistry/immunofluorescence, Western blot and RT-qPCR. By contrast, poly I:C pretreatment markedly reversed the DSS-induced up-regulated expressions of the inflammatory cytokines TNF-α, IL-17 and IFN-γ.

CONCLUSION

Our study suggested that poly I:C may protect against DSS-induced colitis through maintaining integrity of the epithelial barrier and regulating innate immune responses, which may shed light on the therapeutic potential of poly I:C in human colitis.

Authors+Show Affiliations

Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28246473

Citation

Zhao, Hong-Wei, et al. "Effect of Toll-like Receptor 3 Agonist Poly I:C On Intestinal Mucosa and Epithelial Barrier Function in Mouse Models of Acute Colitis." World Journal of Gastroenterology, vol. 23, no. 6, 2017, pp. 999-1009.
Zhao HW, Yue YH, Han H, et al. Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis. World J Gastroenterol. 2017;23(6):999-1009.
Zhao, H. W., Yue, Y. H., Han, H., Chen, X. L., Lu, Y. G., Zheng, J. M., Hou, H. T., Lang, X. M., He, L. L., Hu, Q. L., & Dun, Z. Q. (2017). Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis. World Journal of Gastroenterology, 23(6), 999-1009. https://doi.org/10.3748/wjg.v23.i6.999
Zhao HW, et al. Effect of Toll-like Receptor 3 Agonist Poly I:C On Intestinal Mucosa and Epithelial Barrier Function in Mouse Models of Acute Colitis. World J Gastroenterol. 2017 Feb 14;23(6):999-1009. PubMed PMID: 28246473.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis. AU - Zhao,Hong-Wei, AU - Yue,Yue-Hong, AU - Han,Hua, AU - Chen,Xiu-Li, AU - Lu,Yong-Gang, AU - Zheng,Ji-Min, AU - Hou,Hong-Tao, AU - Lang,Xiao-Meng, AU - He,Li-Li, AU - Hu,Qi-Lu, AU - Dun,Zi-Qian, PY - 2016/08/17/received PY - 2016/09/26/revised PY - 2016/10/30/accepted PY - 2017/3/2/entrez PY - 2017/3/2/pubmed PY - 2017/8/12/medline KW - Dextran sulfate sodium-induced acute colitis KW - Epithelial barrier disruption KW - Mucosal injury KW - Poly I:C KW - Tight junction SP - 999 EP - 1009 JF - World journal of gastroenterology JO - World J. Gastroenterol. VL - 23 IS - 6 N2 - AIM: To investigate potential effects of poly I:C on mucosal injury and epithelial barrier disruption in dextran sulfate sodium (DSS)-induced acute colitis. METHODS: Thirty C57BL/6 mice were given either regular drinking water (control group) or 2% (w/v) DSS drinking water (model and poly I:C groups) ad libitum for 7 d. Poly I:C was administrated subcutaneously (20 μg/mouse) 2 h prior to DSS induction in mice of the poly I:C group. Severity of colitis was evaluated by disease activity index, body weight, colon length, histology and myeloperoxidase (MPO) activity, as well as the production of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin 17 (IL-17) and interferon-γ (IFN-γ). Intestinal permeability was analyzed by the fluorescein isothiocyanate labeled-dextran (FITC-D) method. Ultrastructural features of the colon tissue were observed under electron microscopy. Expressions of tight junction (TJ) proteins, including zo-1, occludin and claudin-1, were measured by immunohistochemistry/immunofluorescence, Western blot and real-time quantitative polymerase chain reaction (RT-qPCR). RESULTS: DSS caused significant damage to the colon tissue in the model group. Administration of poly I:C dramatically protected against DSS-induced colitis, as demonstrated by less body weight loss, lower disease activity index score, longer colon length, colonic MPO activity, and improved macroscopic and histological scores. It also ameliorated DSS-induced ultrastructural changes of the colon epithelium, as observed under scanning electron microscopy, as well as FITC-D permeability. The mRNA and protein expressions of TJ protein, zo-1, occludin and claudin-1 were also found to be significantly enhanced in the poly I:C group, as determined by immunohistochemistry/immunofluorescence, Western blot and RT-qPCR. By contrast, poly I:C pretreatment markedly reversed the DSS-induced up-regulated expressions of the inflammatory cytokines TNF-α, IL-17 and IFN-γ. CONCLUSION: Our study suggested that poly I:C may protect against DSS-induced colitis through maintaining integrity of the epithelial barrier and regulating innate immune responses, which may shed light on the therapeutic potential of poly I:C in human colitis. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/28246473/Effect_of_toll_like_receptor_3_agonist_poly_I:C_on_intestinal_mucosa_and_epithelial_barrier_function_in_mouse_models_of_acute_colitis_ L2 - http://www.wjgnet.com/1007-9327/full/v23/i6/999.htm DB - PRIME DP - Unbound Medicine ER -