Rat Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) in Inflammation

Handa, Osamu; Naito, Yuji; Yoshikawa, Toshikazu

doi:10.3164/jcbn.38.51

Cited by 25 publications

(18 citation statements)

References 58 publications

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“…For neutrophils, it is the result of excessive defense reactions of the human body against H. pylori intrusion, and for H. pylori, it is a convenient tool for invading the human gastric mucosa. Although the role of H. pyloriinduced oxidative stress in gastric epithelial cells is not clear, it might be involved in signal transduction in epithelial cells [20,21], or in gastric carcinogenesis. Further study is required to elucidate the role of H. pylori-induced oxidative stress in gastric epithelial cells and gastric carcinogenesis.…”

Section: Ros/rns Production In H Pylori-infected Gastric Mucosamentioning

confidence: 99%

Helicobacter pylori: a ROS-inducing bacterial species in the stomach

2010

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Section: Ros/rns Production In H Pylori-infected Gastric Mucosamentioning

confidence: 99%

Helicobacter pylori: a ROS-inducing bacterial species in the stomach

2010

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“…It is speculated that neutrophils are activated by and react to microcirculation injury by rolling, adhesion, extravasation, and infiltration into a site via adhesion molecules induced by inflammatory cytokines and that mediators released from activated neutrophils induce organ injury [15,16] . Thus, inflammatory cytokines, in particular IL-8, are greatly involved [17,18] , and the roles of IL-8 in the pathogenesis of ischemia-reperfusion injuries have been investigated by using anti-IL-8 antibodies [19] .…”

Section: Controlmentioning

confidence: 99%

Bacterial Translocation in Small Intestinal Ischemia-Reperfusion Injury and Efficacy of Anti-CINC Antibody Treatment

Kaneko¹,

Tamura²,

Ishii³

et al. 2007

Eur Surg Res

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The involvement of bacterial translocation in small intestinal ischemia-reperfusion injuries and the efficacy of using anti-CINC antibodies for treatment were investigated. A model for ischemia-reperfusion injury of the small intestine was constructed by clamping the supramesenteric artery (for 90 min) in rats. Anti-CINC antibodies and saline were given just before the induction of ischemia in the treatment group and the control group, respectively. Six hours after reperfusion, bacteria were detected in the mesenteric lymph nodes, but the ‘bacteria-positive’ rate was significantly lower in the treatment group than in the control group. Bacterial cultures and endotoxins in the blood were negative in both groups up to 24 h later. The plasma cytokine levels showed similar variations, although the increases were significantly lower after reperfusion in the treatment group. In addition, the degrees of neutrophil infiltration and mucosal injury were attenuated in the small intestine, and the structure of the liver was maintained. Furthermore, the 1-week survival was improved. These results suggest that bacterial translocation occurred predominantly via the lymphatic system and that anti-CINC antibody treatment exerted a protective effect against small intestinal ischemia-reperfusion injury.

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“…Thrombin is known to have inflammatory functions via G protein-coupled receptors, including proteaseactivated receptor-1 (PAR1) (3,15). It has been reported that PAR1 induces rat cytokine-induced neutrophil chemoattractant-1 (CINC-1), a CXC chemokine of the interleukin-8 family (7,8), release (30) and that thrombin stimulates proinflammatory production in vivo (31) and in vitro (4,20,28). However, the role of the thrombin/PAR1 pathway in intestinal I-R has not yet been investigated.…”

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Role of the thrombin/protease-activated receptor 1 pathway in intestinal ischemia-reperfusion injury in rats

Tsuboi

Naito²,

Katada³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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CXC chemokines, including human interleukin-8 and rat cytokine-induced neutrophil chemoattractant-1, play a crucial role in the pathogenesis of intestinal inflammation induced by ischemia-reperfusion (I-R). Thrombin and its specific receptor, protease-activated receptor 1 (PAR1), act as important players in inflammation. However, the association between thrombin activation and chemokine production during I-R has not been well studied. We investigated whether thrombin and PAR1 might be involved in the pathophysiology of intestinal I-R, using an in vivo model. Intestinal damage was induced by clamping the superior mesenteric artery for 30 min followed by reperfusion in male Wistar rats. Thrombin-antithrombin complex was measured as an indicator of thrombin activation. PAR1 expression in the intestine was evaluated by real-time PCR. The severity of the intestinal mucosal injury was evaluated on the distal segment of the ileum by several biochemical markers and histological findings. Reperfusion significantly increased the serum levels of thrombin-antithrombin complex and enhanced PAR1 expression in the intestinal mucosa. The levels of both intraluminal hemoglobin and protein were significantly increased in the I-R group. The mucosal myeloperoxidase activity and expressions and/or productions of cytokine-induced neutrophil chemoattractant-1 and TNF-alpha were significantly increased after I-R. These increases were inhibited by the treatment of rat with antithrombin intravenously before I-R at a dose of 30 U/kg. These results suggest that the thrombin/PAR1 pathway plays an important role in the production of these cytokines during I-R and that antithrombin exerts potent anti-inflammatory effects on this injury via inhibition of proinflammatory cytokines.

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Rat Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) in Inflammation

Cited by 25 publications

References 58 publications

Helicobacter pylori: a ROS-inducing bacterial species in the stomach

Helicobacter pylori: a ROS-inducing bacterial species in the stomach

Bacterial Translocation in Small Intestinal Ischemia-Reperfusion Injury and Efficacy of Anti-CINC Antibody Treatment

Role of the thrombin/protease-activated receptor 1 pathway in intestinal ischemia-reperfusion injury in rats

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