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

@article{Yang2003IL6IE,
  title={IL-6 is essential for development of gut barrier dysfunction after hemorrhagic shock and resuscitation in mice.},
  author={Runkuan Yang and Xiaonan Han and Takashi Uchiyama and Simon Watkins and Arino Yaguchi and Russell L. Delude and Mitchell P. Fink},
  journal={American journal of physiology. Gastrointestinal and liver physiology},
  year={2003},
  volume={285 3},
  pages={
          G621-9
        }
}
  • R. Yang, Xiaonan Han, +4 authors M. Fink
  • Published 1 September 2003
  • Biology
  • American journal of physiology. Gastrointestinal and liver physiology
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… 
View on PubMed
ajpgi.physiology.org
163 Citations
Highly Influential Citations
6
Background Citations
62
Methods Citations
7
Results Citations
5

Figures from this paper

163 Citations

Citation Type

Citation Type

The role of RAGE in the pathogenesis of intestinal barrier dysfunction after hemorrhagic shock.
TLDR
HS/R induced bacterial translocation, ileal mucosal hyperpermeability, and high plasma IL-6 levels in rage(+/+) but not rage(-/-) mice, and activation of RAGE-dependent signaling is a key factor leading to gut mucosal barrier dysfunction after HS/R.
Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock
TLDR
The notion that HMGB1 is a mediator of HS/R-induced gut barrier dysfunction is supported and anti-HMGB1 antibodies warrant further evaluation as a therapeutic to ameliorate the morbidity ofHS/R in trauma patients is suggested.
INTESTINE-SPECIFIC OVEREXPRESSION OF IL-10 IMPROVES SURVIVAL IN POLYMICROBIAL SEPSIS
TLDR
It is indicated that gut-specific overexpression of IL-10 improves survival in a murine model of sepsis, and interactions between the intestinal epithelium and the systemic immune system may play a role in conferring this survival advantage.
Maladaptive role of IL-6 in ischemic acute renal failure.
TLDR
In situ hybridization and immunohistochemistry showed that macrophages infiltrated areas adjacent to the vascular bundles in the outer medulla within hours of reperfusion and showed that these macrophage produced IL-6 mRNA.
Cyclooxygenase-2 Deficiency Leads to Intestinal Barrier Dysfunction and Increased Mortality during Polymicrobial Sepsis
TLDR
The findings reveal that absence of COX-2 is associated with enhanced intestinal epithelial permeability and leads to exaggerated bacterial translocation and increased mortality during peritonitis-induced sepsis.
Burns, inflammation, and intestinal injury: protective effects of an anti-inflammatory resuscitation strategy.
TLDR
PTX attenuates burn-induced intestinal permeability and subsequent intestinal inflammation and may be an ideal candidate for use as an immunomodulatory adjunct to resuscitation fluid.
Effect of BML-111 on the intestinal mucosal barrier in sepsis and its mechanism of action.
TLDR
It was indicated that alterations in the expression of toll-like receptor (TLR)2 and TLR4 may be one of the molecular mechanisms underlying the protective effect of BML-111 on the intestinal mucosal barrier in sepsis.
Increased iNOS Activity is Essential for Intestinal Epithelial Tight Junction Dysfunction in Endotoxemic Mice
TLDR
The view that at least one mechanism contributing to the pathogenesis of gastrointestinal epithelial dysfunction secondary to systemic inflammation is increased iNOS-dependent NO· production leading to altered expression and localization of key TJ proteins is supported.
Beneficial effects of ulinastatin on gut barrier function in sepsis
TLDR
The results suggest that ulinastatin has a therapeutic potential to prevent gut barrier dysfunction in the early stage of sepsis, thereby improving the outcome of septic shock and suggesting a preserved integrity and function of the gut barrier.
Cytokine and radical inhibition in septic intestinal barrier failure.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 63 REFERENCES
Essential role for IL-6 in postresuscitation inflammation in hemorrhagic shock.
TLDR
IL-6 is an essential component of the postresuscitation inflammatory cascade in HS and that the local proinflammatory effects of IL-6 on PMN infiltration and organ damage in HS dominate over the anti- inflammatory effects of systemic IL- 6.
Effect of hemorrhagic shock on gut barrier function and expression of stress-related genes in normal and gnotobiotic mice.
TLDR
The view that the hepatic inflammatory response to HS/R is largely independent of the presence of potentially pathogenic gram-negative bacteria colonizing the gut, whereas the local mucosal response to HSBC is profoundly influenced by the microbial ecology within the lumen during and shortly after the period of hemorrhage is supported.
Intestinal permeability is reduced and IL-10 levels are increased in septic IL-6 knockout mice.
  • Q. Wang, C. Fang, P. Hasselgren
  • Biology, Medicine
    American journal of physiology. Regulatory, integrative and comparative physiology
  • 2001
TLDR
Increased intestinal permeability during sepsis may be regulated by an interaction between IL-6 and IL-10, and treatment with IL- 10 may prevent the increase in mucosal permeabilityDuring sepsi.
Microvascular effects of oral interleukin-6 on ischemia/reperfusion in the murine small intestine.
Increased gut permeability after hemorrhage is associated with upregulation of local and systemic IL-6.
TLDR
The results indicate that lumen-to-blood passage of FD4 through the wall of the small intestine increased significantly at 1.5 h after hemorrhage and resuscitation and was associated with decreased intestinal perfusion and portal blood flow.
IL-6 rescues enterocytes from hemorrhage induced apoptosis in vivo and in vitro by a bcl-2 mediated mechanism.
TLDR
The data show that exposure of intestinal epithelial cells to IL-6 either by oral administration in hemorrhaged mice or by coculture following hypoxia and LPS treatment results in increased bcl-2 gene expression and reduced damage from apoptosis.
Role of interleukin-6 in a non-septic shock model induced by zymosan.
TLDR
It is demonstrated that IL-6 exerts a role in zymosan-induced non-septic shock and in vivo treatment with anti-IL-6 significantly reduced the inflammatory process.
Distinct effects of systemic infusion of G-CSF vs. IL-6 on lung and liver inflammation and injury in hemorrhagic shock.
Production of pro-inflammatory cytokines, such as granulocyte colony-stimulating factor (G-CSF) and interleukin-6 (IL-6) occurs at multiple tissue sites in hemorrhagic shock (HS), resulting in…
Effects of antimurine interleukin-6 on bacterial translocation during gut-derived sepsis.
TLDR
Improved outcome was associated with a reduction of IL-6 levels by anti-IL-6 antibody and appears to play a major role in both the intensity of translocation of E coli from the intestine following burn injury and the host's ability to kill translocated organisms.
Interleukin-6 production in hemorrhagic shock is accompanied by neutrophil recruitment and lung injury.
TLDR
Findings indicate that IL-6 production and Stat3 activation occur early in HS and may contribute to PMN-mediated lung injury, including ARDS after HS.
...
1
2
3
4
5
...