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Effects of Toxin A from Clostridium difficile on Mast Cell Activation and Survival

机译：艰难梭菌毒素A对肥大细胞活化和存活的影响

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Toxins A and B from Clostridium difficile are the main cause of antibiotic-associated diarrhea and pseudomembranous colitis. They cause fluid accumulation, necrosis, and a strong inflammatory response when inoculated in intestinal loops. Since mast cells are a rich source of inflammatory mediators, abundant in the gut, and known to be involved in C. difficile-induced enteritis, we studied the in vitro effect of toxin A on isolated mast cells. Normal rats sensitized by infection with Nippostrongilus brasiliensis were used to isolate peritoneal mast cells (PMC). PMC from naive rats were stimulated with calcium ionophore A23187 as a model of antigen-independent activation, and PMC from sensitized rats were stimulated with N. brasiliensis antigens to study immunoglobulin E-dependent mast cell activation. After 4 h, toxin A did not induce release of nitric oxide or histamine in naive PMC. However, 10 ng of toxin per ml caused a significant release of tumor necrosis factor alpha (TNF-α). In contrast, 1 μg of toxin per ml inhibited antigen or A23187-induced histamine release by PMC. Toxin A at 1 μg/ml for 4 h caused disruption of actin which aggregated in the cytoplasm and around the nucleus. After 24 h, chromatin condensation, cytoplasmic blebbing, and apoptotic-like vesicles were observed; DNA fragmentation was documented also. These results suggest that mast cells may participate in the initial inflammatory response toC. difficile infection by releasing TNF-α upon interaction with toxin A. However, longer exposure to toxin A affects the release of inflammatory mediators, perhaps because of the alteration of the cytoskeleton and induction of apoptosis. The impaired functions and survival of mast cells by C. difficile toxin A could hamper the capacity of these cells to counteract the infection, thus prolonging the pathogenic effects of C. difficiletoxins.
机译：艰难梭菌的毒素A和B是引起抗生素相关性腹泻和假膜性结肠炎的主要原因。当接种在肠loop中时，它们会引起积液，坏死和强烈的炎症反应。由于肥大细胞是炎性介质的丰富来源，在肠道中含量很高，并且已知与 C有关。难治性肠炎，我们研究了毒素A对离体肥大细胞的体外作用。用感染巴西 strong> Nippostrongilus brasiliensis 的正常大鼠分离腹膜肥大细胞（PMC）。用钙离子载体A23187刺激天真大鼠的PMC作为抗原非依赖性激活模型，用 N刺激致敏大鼠的PMC。 Brasiliensis 抗原来研究免疫球蛋白E依赖性肥大细胞的活化。 4小时后，毒素A并未诱导幼稚PMC中一氧化氮或组胺的释放。但是，每毫升10 ng毒素会导致肿瘤坏死因子α（TNF-α）大量释放。相反，每毫升1μg毒素可抑制PMC抗原或A23187诱导的组胺释放。 1μg/ ml的毒素A持续4 h会破坏肌动蛋白，肌动蛋白聚集在细胞质中和细胞核周围。 24小时后，观察到染色质浓缩，细胞质起泡和凋亡样小泡。还记录了DNA片段化。这些结果表明肥大细胞可能参与了对C的初始炎症反应。通过与毒素A相互作用释放TNF-α引起的艰难梭菌感染。然而，长时间暴露于毒素A会影响炎症介质的释放，这可能是由于细胞骨架的改变和细胞凋亡的诱导。 C对肥大细胞功能和存活的损害。艰难梭菌毒素A可能会阻碍这些细胞抵抗感染的能力，从而延长 C的致病作用。难消化毒素。

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