1998
DOI: 10.1046/j.1365-2168.1998.00867.x
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Sodium fusidate and the cytokine response in an experimental model of acute pancreatitis

Abstract: Pretreatment with sodium fusidate resulted in a considerable reduction in mortality rate and ascitic fluid output in rabbits with bile-induced ANP, probably by lowering the TNF-alpha and IL-8 blood levels. However, pretreatment with sodium fusidate did not alter the local or systemic manifestations of ANP. Thus, cytokines other than TNF-alpha and IL-8 are likely to mediate the local and systemic symptoms of ANP.

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Cited by 12 publications
(5 citation statements)
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“…In an experimental model of pancreatitis, fusidin has also been shown to reduce the blood levels of the neutrophil chemoattractrant chemokine IL-8 [48] in treated animals as compared to controls [26]. However, because neither the role of IL-8 nor of other chemokines has been yet been studied in GBS/EAN it is difficult to predict if and how reduction in IL-8 production in rat EAN may have further contributed to the beneficial effects of fusidin in this setting.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In an experimental model of pancreatitis, fusidin has also been shown to reduce the blood levels of the neutrophil chemoattractrant chemokine IL-8 [48] in treated animals as compared to controls [26]. However, because neither the role of IL-8 nor of other chemokines has been yet been studied in GBS/EAN it is difficult to predict if and how reduction in IL-8 production in rat EAN may have further contributed to the beneficial effects of fusidin in this setting.…”
Section: Discussionmentioning
confidence: 99%
“…Accordingly, this drug ameliorates the course of several immunoinflammatory diseases such as chronic endogenous uveitis [16], type 1 diabetes [17][18][19][20], Bechet's colitis [21], Crohn's disease [22], immunoinflammatory hepatitis [23], sepsis [24,25] and pancreatitis [26] in humans and/or animal models. Of particular interest here is the observation of one patient with GBS who has apparently benefitted from fusidin [27].…”
Section: Introductionmentioning
confidence: 99%
“…The interference of fusidin with the cytokine network may however be more pronounced and more complex than anticipated from in-vitro studies, and administering fusidin to endotoxin-or Concanavalin (Con) A-challenged rodents markedly suppresses the blood levels of TNF-and augments those of IL-6 [29][30][31][32]. This immunopharmacological profile of fusidin may be related to its beneficial effects in type 1 cytokinedependent diseases such as type 1 DM [29,[33][34][35], chronic endogenus uveitis [36], Guillain Barré syndrome [37][38], multiple sclerosis [39], Beçhet's colitis [40], Crohn's disease [41], systemic sclerosis [42], immunoinflammatory hepatitis [32], pancreatitis [43] and sepsis [29,31] in humans and/or in animal models. The potential clinical relevance of fusidin in the treatment of immunoinflammatory diseases is underscored by its use for many years as an antibiotic with only minor and reversible side effects [27].…”
Section: Introductionmentioning
confidence: 99%
“…This clinical and histological study adds the monophasic model of EAE to the increasing list of immunoin¯ammatory and autoimmune diseases that respond favorably to fusidin. Other diseases ± in humans and/or in animal models ± include chronic endogenous uveitis, 19 type 1 diabetes mellitus, 10,16,20 ± 21 Bechet's colitis, 22 Crohn's disease, 23 hepatitis, 13 pancreatitis, 15 sclerodermia, 24 and the Guillain Barre  syndrome. 14,25 These data, along with the minimal and reversible toxicity of fusidin 8 and its capacity to penetrate the blood ± brain barrier, 26 suggest that the drug might be used in the treatment of MS patients.…”
Section: Discussionmentioning
confidence: 99%