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

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...

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Bibliographic Details
Published in:American journal of physiology: Gastrointestinal and liver physiology 2003-09, Vol.285 (3), p.G621-G629
Main Authors: Yang, Runkuan, Han, Xiaonan, Uchiyama, Takashi, Watkins, Simon K, Yaguchi, Arino, Delude, Russell L, Fink, Mitchell P
Format: Article
Language:English
Subjects:
Alanine Transaminase - blood
Animals
Cytokines - genetics
Gene Expression
Interleukin-10 - blood
Interleukin-6 - metabolism
Intestines - metabolism
Male
Membrane Proteins - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Permeability
Resuscitation
Shock, Hemorrhagic - genetics
Shock, Hemorrhagic - metabolism
Shock, Hemorrhagic - therapy
Tight Junctions - metabolism
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Summary: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.
ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.00177.2003