Visceral Ischemia-Reperfusion Injury Promotes Tumor Necrosis Factor (Tnf) and Interleukin-1 (Il-1) Dependent Organ Injury in the Mouse

Welborn, M. Burress; Douglas, Wade G.; Abouhamze, Zaher; Auffenburg, Troy; Abouhamze, Amer; Baumhofer, Julie; Seeger, James M.; Pruitt, Jeffrey H.; Edwards, Paul D.; Chizzonite, R; Martin, David; Moldawer, Lyle L.; Harward, Timothy R.S.

doi:10.1097/00024382-199609000-00003

Cited by 38 publications

(28 citation statements)

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“…12 However, in an experimental study with 30 minutes of supraceliac aortic clamping, lung performance was significantly improved by neutralization of TNF or IL-1, which suggests that both of these mediators contributed to the disturbed homeostasis after TAAA repair. 15 The present data highlight complement as a possible inducer of the proinflammatory response after TAAA repair and complement inhibition as a possible therapeutic approach in this condition.…”

Section: Discussionmentioning

confidence: 67%

“…[12][13][14][15] Despite substantial evidence of the importance of complement in experimental ischemia-reperfusion injury, there are no published data on the occurrence and possible consequences of complement activation after TAAA. The aim of the present study was to elucidate the degree and mechanism of complement activation during and after TAAA repair and to relate this activation to other aspects of the inflammatory response.…”

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confidence: 99%

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Mechanism of Complement Activation and Its Role in the Inflammatory Response After Thoracoabdominal Aortic Aneurysm Repair

et al. 2003

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Background-Complement activation contributes to ischemia-reperfusion injury. Patients undergoing thoracoabdominal aortic aneurysm (TAAA) repair suffer extensive ischemia-reperfusion and considerable systemic inflammation. Methods and Results-The degree and mechanism of complement activation and its role in inflammation were investigated in 19 patients undergoing TAAA repair. Patients undergoing open infrarenal aortic surgery (nϭ5) or endovascular descending aortic aneurysm repair (nϭ6) served as control subjects. Substantial complement activation was seen in TAAA patients but not in controls. C1rs-C1-inhibitor complexes increased moderately, whereas C4bc, C3bBbP, C3bc, and the terminal SC5b-9 complex (TCC) increased markedly after reperfusion, reaching a maximum 8 hours after reperfusion. Interleukin (IL)-1␤, tumor necrosis factor ␣ (TNF-␣), and IL-8 increased significantly in TAAA patients but not in controls, peaking at 24 hours postoperatively and correlating closely with the degree of complement activation. IL-6 and IL-10 increased to a maximum 8 hours after reperfusion in the TAAA patients, were not correlated with complement activation, and increased moderately in the control subjects. Myeloperoxidase and lactoferrin increased markedly before reperfusion in all groups, whereas sICAM-1, sP-selectin, and sE-selectin were unchanged.No increase was observed in complement activation products, IL-1␤, TNF-␣, or IL-8 in a mannose-binding lectin (MBL)-deficient TAAA patient, whereas IL-6, IL-10, myeloperoxidase, and lactoferrin increased as in the controls. Two other MBL-deficient TAAA patients receiving plasma attained significant MBL levels and showed complement and cytokine patterns identical to the MBL-sufficient TAAA patients. Conclusions-The data suggest that complement activation during TAAA repair is MBL mediated, amplified through the alternative pathway, and responsible in part for the inflammatory response.

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Section: Discussionmentioning

confidence: 67%

mentioning

confidence: 99%

Mechanism of Complement Activation and Its Role in the Inflammatory Response After Thoracoabdominal Aortic Aneurysm Repair

et al. 2003

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“…9) Ding et al 14) and Appleyard et al 15) reported that plasma TNF a level was increased significantly after indomethacin administration, and suggested that TNF a plays a critical role in indomethacin-induced gastric mucosal damage. Welborn et al 16) and Garcia- IL-1 concentration was measured at 30 min after indomethacin administration. Each value is the meanϮS.E.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Superoxide Generation System in Indomethacin-Induced Gastric Mucosal Injury in Rats.

Tanaka¹,

Yuda²,

Yamakawa

2001

Biological & Pharmaceutical Bulletin

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Indomethacin and several other nonsteroidal anti-inflammatory drugs (NSAID) are known to produce gastric mucosal injury.1,2) The pathogenesis of NSAID-induced gastric mucosal injury is reported for inhibition of prostaglandin (PG) biosynthesis 3) and depletion of gastric mucosal blood flow. 4,5) A number of studies have highlighted the importance of alterations in mucosal blood flow after NSAID administration. By this depletion of gastric mucosal blood flow, polymorphonuclear leukocytes (PMN) were infiltlated to gastric mucosal tissue. 6) We clarified these phenomena that PMN infiltlates, generates oxygen radicals and induces direct gastric mucosal injury, and then increasing lipid peroxidation further aggravate damage in previous study. 7) We demonstrated that neutrophil-derived free radicals are also important factors in the gastric mucosal injury induced ischemia-reperfusion in pylorus-ligated rats.8) But the generation system of oxygen free radicals is not clear in the indomethacin induced-gastric mucosal injury. We examined this and report here the mechanism of pathogenesis in this type of injury.Superoxide radicals have several generation systems, with activation of xanthine-xanthine oxidase (XOD) enzyme in vein cellular tissue and activation of NADPH oxidase enzyme in PMN being the main ones. The direct effect of indomethacin on XOD activity in vitro and NADPH oxidase in ex vivo was therefore examined.Cytokines, IL-1 and TNF a are well known to play important roles in inflammation.9) The first step of PMN infiltration into an inflammation site is believed to take place in many cytokines and the growth binding factors IL-1 and TNF a from mast cells and macrophages. We measured cytokines to learn whether indomethacin acts to directly activate the oxygen radical generation system or is a second any effect. MATERIALS AND METHODS AnimalsMale Donryu rats (SPF) 8 weeks old were obtained from Charles River Co., Tokyo, and ICR mice (SPF) 8 weeks old were obtained from SLC Japan Co., Tokyo.Materials Indomethacin, ferricytochrome C (horse heart type III), NADPH Na (type III), NBT and BCIP were obtained from Sigma, and xanthine oxidase solution from Boehringer Mannheim Yamanouchi, Tokyo. Diphenylene iodonium chloride was from ALEXIS Co., U.S.A.; Bio-Rad protein assay was from BIO RAD; anti p47 phox was from Trunsduction Laboratories and mouse IL-1 and the TNF a assay system were obtained from Genzyme. Other chemicals were of reagent grade and were used without purification.Assay of Xanthine Oxidase (XOD) Activity XOD reduced cytochrome c was monitored spectrophotometrically at 550 nm. The reaction mixture consisted of 100 mM potassium phosphate buffer (pH 7.4) (1.2 ml), 0.1 mM cytochrome c (0.2 ml), 5 mM xanthine (0.2 ml) and 0.1 U/ml xanthine oxidase solution (0.2 ml). This mixture was preincubated for 5 min at 37°C and indomethacin was added at a fianl concentration of 0.1, 0.5, 1, 5, or 10 mM. Indomethacin was disorbed by 100% ethanol solution and finally diluted with distilled water at Ͻ1% ethanol concentration.G...

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“…Hepatic neutrophil sequestration was quantitated by measuring tissue levels of myeloperoxidase content as previously described (40). Snap-frozen livers (Ϫ80°C) were weighed and homogenized for 1 min in five parts volume per weight of 0.01 M KH2PO4 with 1 mM EDTA (PE buffer).…”

Section: Myeloperoxidase Activitymentioning

confidence: 99%

LPS-binding protein mediates LPS-induced liver injury and mortality in the setting of biliary obstruction

Minter¹,

Bi²,

Ben-Josef³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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GL. LPS-binding protein mediates LPS-induced liver injury and mortality in the setting of biliary obstruction. Am J Physiol Gastrointest Liver Physiol 296: G45-G54, 2009. First published October 23, 2008 doi:10.1152/ajpgi.00041.2008.-It is generally accepted that low levels of lipopolysaccharide (LPS)-binding protein (LBP) augment the cell's response to LPS, whereas high levels of LBP have been shown to inhibit cell responses to LPS. Clinical studies and in vitro work by our group have demonstrated that, in the setting of liver disease, increased or acute-phase levels of LBP may actually potentiate rather than inhibit an overwhelming proinflammatory response. Therefore, in the present studies we sought to determine the role of acute-phase LBP in mediating morbidity and mortality in animals challenged with LPS in the setting of biliary obstruction. Using LBP-deficient mice and LBP blockade in wild-type mice, we demonstrate that high levels of LBP are deleterious in the setting of cholestasis. Following biliary obstruction and intraperitoneal LPS challenge, hepatic injury, hepatic neutrophil infiltration, and mortality were significantly increased in animals with an intact LBP acute-phase response. Kupffer cell responses from these animals demonstrated a significant increase in several inflammatory mediators, and Kupffer cell-associated LBP appears to be responsible for these differences, at least in part. Our results indicate that the role of LBP signaling in inflammatory conditions is complex and heterogeneous, and elevated levels of LBP are not always protective. Increased LBP production in the setting of cholestatic liver disease appears to be deleterious and may represent a potential therapeutic target for preventing overwhelming inflammatory responses to LPS in this setting.

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Visceral Ischemia-Reperfusion Injury Promotes Tumor Necrosis Factor (Tnf) and Interleukin-1 (Il-1) Dependent Organ Injury in the Mouse

Cited by 38 publications

References 0 publications

Mechanism of Complement Activation and Its Role in the Inflammatory Response After Thoracoabdominal Aortic Aneurysm Repair

Mechanism of Complement Activation and Its Role in the Inflammatory Response After Thoracoabdominal Aortic Aneurysm Repair

Mechanism of Superoxide Generation System in Indomethacin-Induced Gastric Mucosal Injury in Rats.

LPS-binding protein mediates LPS-induced liver injury and mortality in the setting of biliary obstruction

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