IL-6 is essential for development of gut barrier dysfunction after hemorrhagic shock and resuscitation in mice

作者：Runkuan Yang, Xiaonan Han, Takashi Uchiyama, Simon K. Watkins, Arino Yaguchi, Russell L. Delude, Mitchell P. Fink · 发表于：American Journal of Physiology-Gastrointestinal and Liver Physiology · 年份：2003 · DOI：10.1152/ajpgi.00177.2003 · 被引用次数：188 · 研究领域：Barrier Structure and Function Studies、Enhanced Recovery After Surgery、Gut microbiota and health

We sought to determine the role of IL-6 as a mediator of the alterations in gut barrier function that occur after hemorrhagic shock and resuscitation (HS/R). C57Bl/6 wild-type (WT) and IL-6 knockout (KO) mice on a C57Bl/6 background were subjected to either a sham procedure or HS/R. Organ and tissue samples were obtained 4 h after resuscitation. In WT mice, HS/R significantly increased ileal mucosal permeability to fluorescein isothiocyanate-labeled dextran (average molecular mass, 4 kDa) and bacterial translocation to mesenteric lymph nodes. These alterations in gut barrier function were not observed in IL-6 KO animals. HS/R increased ileal steady-state mRNA levels for IL-6, TNF, and IL-10 in WT but not in IL-6 KO mice. Ileal mucosal expression of the tight junction protein, ZO-1, decreased after HS/R in WT but not IL-6 KO mice. Collectively, these data support the view that expression of IL-6 is essential for the development of gut barrier dysfunction after HS/R.