CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin/ICAM-1 deficient mice

Monson, Keith M.; Dowlatshahi, Shadi; Crockett, Elahé T

doi:10.1186/1476-9255-4-11

Cited by 23 publications

(28 citation statements)

References 48 publications

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“…Crockett et al [49] recently showed that significant neutrophil infiltration can occur in P-selectin and ICAM-1 null mice, suggesting that alternative adhesion recruitment pathways independent of adhesion molecule expression do exist and can participate in neutrophil migration during an inflammatory response. Additional studies in mice have indicated that while adhesion molecules are important modulators of neutrophil infiltration, the mode of stimuli and duration of the injury can modulate neutrophil infiltration via the expression of chemotactic cytokines or CXC-chemokines, such as interleukin-8 (IL-8), that may play an equally central role in recruitment and migration [50]. Further studies supporting the importance of chemokines in leukocyte recruitment into inflamed ileal pouch tissue of CUC patients who have undergone IPAA demonstrated that the expression of monocyte chemotactic protein-1 and 3, as well as IL-8, were significantly elevated during episodes of acute ileal inflammation compared with the normal pouch ileum [51].…”

Section: Discussionmentioning

confidence: 99%

Stasis Predisposes Ileal Pouch Inflammation in a Rat Model of Ileal Pouch-Anal Anastomosis

Stucchi

Shebani

Reed

et al. 2010

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Stasis Predisposes Ileal Pouch Inflammation in a Rat Model of Ileal Pouch-Anal Anastomosis

Stucchi

Shebani

Reed

et al. 2010

Journal of Surgical Research

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“…However, the concentration of MDA was obviously lower in the melatonin exposure group than in the other two control groups 6, 12 and 24 h after reperfusion, indicating that melatonin can relieve the IR injury by eliminating free radicals [22] . It was reported that ICAM-1 is directly correlated with the inflammation of white blood cells and vascular endothelial cells [23] . In this study, ICAM-1 gradually increased after reperfusion and decreased after reaching its peak between 12 and 24 h, which was in accordance with the concentration of TNF-α in systemic circulation.…”

Section: Applicationsmentioning

confidence: 99%

Melatonin protects liver from intestine ischemia reperfusion injury in rats

Li¹,

Yin²,

Gu³

et al. 2008

WJG

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AIM:To investigate the protective effect of melatonin on liver after intestinal ischemia-reperfusion injury in rats. METHODS: One hundred and fifty male Wistar rats, weighing 190-210 g, aged 7 wk, were randomly divided into melatonin exposure group, alcohol solvent control group and normal saline control group. Rats in the melatonin exposure group received intraperitoneal (IP) melatonin (20 mg/kg) 30 min before intestinal ischemia-reperfusion (IR), rats in the alcohol solvent control group received the same concentration and volume of alcohol, and rats in the normal saline control group received the same volume of normal saline. Serum samples were collected from each group 0.5, 1, 6, 12, and 24 h after intestinal IR. Levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured with an auto-biochemical analyzer. Serum TNF-α was tested by enzyme-linked immunosorbent assay (ELISA). Malondialdehyde (MDA) in liver was detected by colorimetric assay. Pathological changes in liver and immunohistochemical straining of ICAM-1 were observed under an optical microscope. RESULTS: The levels of ALT measured at various time points after intestinal IR in the melatonin exposure group were significantly lower than those in the other two control groups (P < 0.05). The serum AST levels 12 and 24 h after intestinal IR and the ICAM-1 levels (%) 6, 12 and 24 h after intestinal IR in the melatonin exposure group were also significantly lower than those in the other two control groups (P < 0.05). CONCLUSION: Exotic melatonin can inhibit the activity of ALT, AST and TNF-α, decrease the accumulation of MDA, and depress the expression of ICAM-1 in liver after intestinal IR injury, thus improving the liver function.

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“…It’s possible that KC receptors are not up regulated in the skeletal muscle of the non hypercholesterolemic C57BL6 mice so that KC synthesized in the skeletal muscle of mice subjected to demand ischemia could be released into the systemic circulation. While there is substantial data to support KC release from exercised muscle (35, 36), it is also possible that the KC detected in plasma of the C57BL6 mice subjected to demand ischemia was synthesized by cells outside the ischemic limb.…”

Section: Resultsmentioning

confidence: 99%

Divergent systemic and local inflammatory response to hind limb demand ischemia in wild-type and ApoE–/– mice

Crawford

Albadawi

Robaldo

et al. 2013

Journal of Surgical Research

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Introduction Studies were designed to determine whether the ApoE−/− phenotype modulates the local skeletal muscle and systemic inflammatory (plasma) responses to lower extremity demand ischemia. The ApoE−/− phenotype is an experimental model for atherosclerosis in humans. Methods Aged female ApoE −/− and C57BL6 mice underwent femoral artery ligation, then divided into sedentary and demand ischemia (exercise) groups on day 14. Baseline and post exercise limb perfusion and hind limb function were assessed. On day 14, animals in the demand ischemia group underwent daily treadmill exercise through day 28. Sedentary mice were not exercised. On day 28, plasma and skeletal muscle from ischemic limbs were harvested from sedentary and exercised mice. Muscle was assayed for angiogenic and pro-inflammatory proteins, markers of skeletal muscle regeneration, and evidence of skeletal muscle fiber maturation. Results Hind limb ischemia was similar in ApoE −/− and C57 mice prior to the onset of exercise. Under sedentary conditions, plasma VEGF, IL-6, but not KC or MIP-2 were higher in ApoE (P<0.0001). Following exercise, plasma levels of VEGF, KC and MIP-2, but not IL-6 were lower in ApoE (P<0.004). The cytokines KC and MIP-2 in muscle was greater in exercised ApoE−/− mice as compared to C57BL6 mice (p=0.01). Increased PAR activity, and mature muscle regeneration was associated with demand ischemia in the C57BL6 mice as compared to the ApoE −/− mice (p=0.01). Conclusion Demand limb ischemia in the ApoE−/− phenotype exacerbated the expression of select systemic cytokines in plasma and blunted indices of muscle regeneration.

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CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin/ICAM-1 deficient mice

Cited by 23 publications

References 48 publications

Stasis Predisposes Ileal Pouch Inflammation in a Rat Model of Ileal Pouch-Anal Anastomosis

Stasis Predisposes Ileal Pouch Inflammation in a Rat Model of Ileal Pouch-Anal Anastomosis

Melatonin protects liver from intestine ischemia reperfusion injury in rats

Divergent systemic and local inflammatory response to hind limb demand ischemia in wild-type and ApoE–/– mice

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