Sodium fusidate and increased remission rate of insulin-dependent diabetes mellitus

Lack of effect of intermittently administered sodium fusidate in patients with newly diagnosed type 1 diabetes mellitus: the FUSIDM trial

“…The interference of fusidin with the cytokine network has been ascribed to its capacity to protect beta cells from destruction and to its observed beneficial effects in the three most commonly used preclinical models of human type 1 diabetes: the NOD mouse [4], the DP-BB rat [2,5,6] and the mouse made diabetic with multiple low doses of streptozotocin (MLDSZ) [7]. These preclinical studies were corroborated by the beneficial effects of fusidin treatment in an open study conducted in newly diagnosed type 1 diabetes patients [8]. These observations, along with the fact that fusidin has been used for many years as an antibiotic with only negligible and reversible side effects, prompted us to test fusidin as a strategy to preserve beta cell function shortly after onset of type 1 diabetes in a double-blind, placebo-controlled design.…”

Sodium Fusidate Ameliorates the Course of Diabetes Induced in Mice by Multiple Low Doses of Streptozotocin

“…However, whilst cyclosporin A prevents disease development in the DP-BB rats and the NOD mouse [57][58][59], it exacerbates SZ-induced DM [60]. On the basis of the beneficial effect of fusidin in a small number of patients with newly diagnosed type 1 DM [35] and its minimal toxicity [27], we find double-blind studies with fusidin warranted both in individuals at high risk of developing type 1 DM and in patients with newly diagnosed disease.…”

“…To complement and extend investigations of the antidiabetogenic effects of fusidin previously observed in humans [35] and in the DP-BB rat and NOD mouse models of type 1 DM [29,[33][34], we have conducted the present study in SZ-induced DM. The results show that fusidin ameliorates both the clinical and histological parameters of the disease in a long-lasting fashion, most likely through an inhibitory action on the synthesis/release of IFN-.…”

“…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].…”

Protection from concanavalin A (Con A)-induced T cell-dependent hepatic lesions and modulation of cytokine release in mice by sodium fusidate

“…The antibiotic fusidic acid and its sodium salt SF were previously found to possess immunomodulatory properties in vitro and in vivo ( [9][10][11][12]16,17], reviewed in [7]). The drug down-regulates IL-2, IFN-g, and, though to a lower extent, IL-1 secretion in vitro and also inhibits the lymphocyte costimulatory activity of IL-1a/b and IL-6 [9].…”