fumonisin/воспаление

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Hydrolyzed fumonisin B1 induces less inflammatory responses than fumonisin B1 in the co-culture model of porcine intestinal epithelial and immune cells.

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Fumonisin B₁ (FB₁), mainly produced by Fusarium verticillioides and Fusarium proliferatum, can be converted to the less toxic metabolite hydrolyzed FB₁ (HFB₁) by enzymatic degradation. The application of an FB₁degrading enzyme as a feed additive

Impact of fumonisin B1 on the production of inflammatory cytokines by gastric and colon cell lines.

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Fumonisins, a family of mycotoxins, are mainly toxic and carcinogenic. The present study was carried out to evaluate fumonisin B1 (FB1) effects on the production of inflammatory cytokines by gastric and colon cell lines. The study was performed on two cell lines under in vitro condition, including

Deletion of IFN-gamma reduces fumonisin-induced hepatotoxicity in mice via alterations in inflammatory cytokines and apoptotic factors.

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Fumonisin B(1) (FB(1)) produces species-specific and organ-specific toxicity, including equine leukoencephalomalacia, porcine pulmonary edema, and hepatic or renal damage in other animals. FB(1) causes inhibition of ceramide synthase, leading to accumulation of free sphingoid bases. We previously

Anti-inflammatory and anti-apoptotic effects of fumonisin B1, an inhibitor of ceramide synthase, in a rodent model of splanchnic ischemia and reperfusion injury.

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Ceramide is a sphingolipid with potent proinflammatory and proapoptotic properties. This study sought to determine whether pharmacological inhibition of ceramide biosynthesis in the intestine attenuates pathophysiological sequelae of shock induced by splanchnic artery occlusion and reperfusion.

Increased expression of CD95-ligand and other apoptotic signaling factors by fumonisin B1, a hepatotoxic mycotoxin, in livers of mice lacking tumor necrosis factor alpha.

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Fumonisin B1 (FB1), a mycotoxin, is a potent inhibitor of ceramide synthase, and produces organ-, species-, and even gender-specific toxic responses in animals. The hepatotoxic response of FB1 in mice involves accumulation of free sphingoid bases and induction of inflammatory cytokines including

Individual and combined effects of fumonisin b1 and moniliformin on clinicopathological and cell-mediated immune response in Japanese quail.

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A total of 390 one-day-old quail chicks (Coturnix coturnix japonica) were divided into 4 groups (3 replicates per treatment), viz. CX, FX, MX, and FM, containing 75, 105, 105, and 105 birds, respectively. Birds in the control group (CX) were fed quail mash alone, whereas birds in group FX were fed

Inflammatory activation of arachidonic acid signaling in murine P388D1 macrophages via sphingomyelin synthesis.

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Ceramide has emerged as an important lipid messenger for many cellular processes triggered via surface receptors. In the present study, inflammatory activation of P388D1 macrophages with bacterial lipopolysaccharide (LPS) and platelet-activating factor (PAF) stimulated a transient accumulation of

Activation of mitogen-activated protein kinase by fumonisin B(1) stimulates cPLA(2) phosphorylation, the arachidonic acid cascade and cAMP production.

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Activation of mitogen-activated protein kinase (MAPK) results in pleiotropic effects such as modulation of the transcription and activation of enzymes involved in signal transduction. One such enzyme is the cytoplasmic phospholipase A(2) (cPLA(2)), which releases arachidonic acid (AA). AA is the

Effect of fumonisin B1 on inducible nitric oxide synthase and cyclooxygenase-2 in LPS-stimulated J774A.1 cells.

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Fumonisin B1 (FB1) is a water-soluble fungal metabolite that elicits a wide spectrum of toxicological effects. Cellular targets of FB1 include immune cells and in particular macrophages. In the present study the cytotoxic effect of FB1 (1-100 microM) was evaluated using a murine macrophage cell line

Experiment to determine limits of tolerance for fumonisin B1 in weaned piglets.

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In Hungary almost 70% of mould-affected maize inspected since 1993 was found to be contaminated with fumonisin B1 (FB1) (mean 2.6-8.65 mg/kg; maximum 9.8-75.1 mg/kg), the degree of this contamination was found to increase from year to year (Fazekas et al., 1997b). In this experiment, in order to

The protective role of liver X receptor (LXR) during fumonisin B1-induced hepatotoxicity.

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Fumonisin B1 (FB1), a congener of fumonisins produced by Fusarium species, is the most abundant and most toxicologically active fumonisin. FB1 causes severe mycotoxicosis in animals, including nephrotoxicity, hepatotoxicity, and disruption of the intestinal barrier. However, mechanisms associated

Involvement of de novo ceramide synthesis in pro-inflammatory adipokine secretion and adipocyte-macrophage interaction.

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Interaction between adipocytes and macrophages has been suggested to play a central role in the pathogenesis of obesity. Ceramide, a sphingolipid de novo synthesized from palmitate, is known to stimulate pro-inflammatory cytokine secretion from multiple types of cells. To clarify whether de novo

The ceramide inhibitor fumonisin B1 mitigates the pulmonary effects of low-dose diesel exhaust inhalation in mice.

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Recent studies have suggested that inhalation of diesel exhaust (DE), a major source of air pollution, results in pulmonary alterations; however, the effects of DE at low concentrations are poorly understood. Therefore, this study was conducted to elucidate the pulmonary effects of low-level

Fumonisin b1 reduces the development of multiple organ failure induced by zymosan in mice.

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Ceramide is a major proapoptotic mediator released in response to numerous stimuli, including oxidative stress and cytokines. The role of ceramide in the pathophysiology of inflammation is just emerging, and the potential relevance of this pathway in nonseptic shock is not known. The aim of this

Sphingolipid changes do not underlie fatty acid-evoked GLUT4 insulin resistance nor inflammation signals in muscle cells.

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Ceramides contribute to obesity-linked insulin resistance and inflammation in vivo, but whether this is a cell-autonomous phenomenon is debated, particularly in muscle, which dictates whole-body glucose uptake. We comprehensively analyzed lipid species produced in response to fatty acids and

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