C1 inhibitor prevents capillary leakage after thermal trauma

Radke, A.; Mottaghy, K.; Goldmann, Christine; Khorram-Sefat, Ramin; Kovacs, Birgit; Janssen, Alfons; Klosterhalfen, B.; Hafemann, B.; Pallua, Norbert; Kirschfink, Michael

doi:10.1097/00003246-200009000-00018

Cited by 57 publications

(34 citation statements)

References 40 publications

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“…Thus, as observed in IR injury, specific natural IgM is required for the full evolution of a burn injury. This finding that cutaneous burns induced a similar pathway to inflammation as had been identified in IR injury suggested also that blood flow might be reduced locally following thermal treatment, a phenomenon also suggested by others (26)(27)(28).…”

Section: Bv-bviii and D)supporting

confidence: 73%

Innate response to self-antigen significantly exacerbates burn wound depth

Suber

Carroll

Moore

2007

Proc. Natl. Acad. Sci. U.S.A.

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A major component of burn injury is caused by additional local damage from acute inflammation. Using a scald burn model in mice, we find that this part of the injury is dependent on recognition of self-antigen by specific natural IgM, leading to activation of the complement system. We propose that the depth of a burn wound is a sum of the thermal energy applied and of the degree of host inflammatory response.complement ͉ natural IgM ͉ trauma ͉ wound physiology

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Section: Bv-bviii and D)supporting

confidence: 73%

Innate response to self-antigen significantly exacerbates burn wound depth

Suber

Carroll

Moore

2007

Proc. Natl. Acad. Sci. U.S.A.

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“…The red cell hemolysis assay was conducted employing a well-established protocol (70). Briefly, freshly collected and carefully washed (3 times) rabbit red blood cells water and for a negative control 300 µl assay buffer were added.…”

Section: Red Blood Cell Hemolysis Assaymentioning

confidence: 99%

The lectin-like domain of thrombomodulin ameliorates diabetic glomerulopathy via complement inhibition

Wang¹,

Vinnikov²,

Shahzad³

et al. 2012

Thromb Haemost

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“…Treatment with C1 inhibitor improves outcome in a number of animal models of inflammatory disease including gram negative bacterial sepsis and endotoxin shock, vascular leak syndromes, hyperacute transplant rejection, and ischemia-reperfusion injury (Akita et al, 2003;Buerke et al, 1995;Buerke et al, 1998;Dalmasso and Platt, 1993;De Simoni et al, 2003;De Simoni et al, 2004a;Fiane et al, 1999;Fukuta et al, 2003;Giebler et al, 1999;Guerrero et al, 1993;Hecker et al, 2002;Henze et al, 1997;Horstick et al, 1997;Horstick et al, 2001a;Jansen et al, 1998;Khorram-Sefat et al, 1998;Matsunami et al, 2000;Nielsen et al, 2002;Przemeck et al, 2002;Radke et al, 2000;Schelzig et al, 2001;Scherer et al, 1996;Schmidt et al, 1999a;Schmidt et al, 1999b) (Table 1). For example, in myocardial ischemia-reperfusion injury, treatment with C1 inhibitor resulted in decreased infarct size, decreased myocardial neutrophil accumulation, decreased plasma levels of creatine kinase, C3a and C5a, and decreased expression of P-selectin and ICAM-1 within the cardiac endothelium (Buerke et al, 1995;Buerke et al, 1998;Horstick et al, 1997;Horstick et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

C1 inhibitor: Biologic activities that are independent of protease inhibition

Davis

Cai

2007

Immunobiology

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C1 inhibitor therapy improves outcome in several animal models of inflammatory disease. These include sepsis and gram negative endotoxin shock, vascular leak syndromes, hyperacute transplant rejection, and ischemia-reperfusion injury. Furthermore, some data suggest a beneficial effect in human inflammatory disease. In many inflammatory conditions, complement system activation plays a role in pathogenesis. The contact system also very likely is involved in mediation of damage in inflammatory disease. Therefore, the beneficial effect of C1 inhibitor has been assumed to result from inhibition of one or both of these systems. Over the past several years, several other potential anti-inflammatory effects of C1 inhibitor have been described. These effects do not appear to require protease inhibition and depend on non-covalent interactions with other proteins, cell surfaces or lipids. In the first, C1 inhibitor binds to a variety of extracellular matrix components including type IV collagen, laminin, entactin and fibrinogen. The biologic role of these reactions is unclear, but they may serve to concentrate C1 inhibitor at extravascular inflammatory sites. The second is a noncovalent interaction with C3b that results in inhibition of formation of the alternative pathway C3 convertase, a function analogous to that of factor H. The third is an interaction with E and P selectins on endothelial cells that is mediated by the Lewis x tetrasaccharides that are expressed on C1 inhibitor. These interactions result in suppression of leukocyte rolling and transmigration. The fourth interaction is the binding of C1 inhibitor to gram negative bacterial endotoxin that results in suppression of endotoxin shock by interference with the interaction of endotoxin with its receptor complex on macrophages. Lastly, C1 inhibitor binds directly to gram negative bacteria, which leads to suppression of the development of sepsis, as demonstrated in the cecal ligation and puncture model. These observations suggest that C1 inhibitor is a multi-faceted anti-inflammatory protein that exerts its effects through a variety of mechanisms including both protease inhibition and several different non-covalent interactions that are unrelated to protease inhibition.

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C1 inhibitor prevents capillary leakage after thermal trauma

Abstract: Application of C1Inh appears to be an effective means to prevent capillary leakage and inflammatory tissue destruction after thermal trauma.

Cited by 57 publications

References 40 publications

Innate response to self-antigen significantly exacerbates burn wound depth

Innate response to self-antigen significantly exacerbates burn wound depth

The lectin-like domain of thrombomodulin ameliorates diabetic glomerulopathy via complement inhibition

C1 inhibitor: Biologic activities that are independent of protease inhibition

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