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首页> 外文期刊>Infection and immunity >Interleukin-4 (IL-4) and IL-13 Suppress Excessive Neutrophil Infiltration and Hepatocyte Damage during Acute Murine Schistosomiasis Japonica
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Interleukin-4 (IL-4) and IL-13 Suppress Excessive Neutrophil Infiltration and Hepatocyte Damage during Acute Murine Schistosomiasis Japonica

机译：白细胞介素4（IL-4）和IL-13抑制急性小鼠日本血吸虫病中性粒细胞浸润和肝细胞损伤。

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Due to the importance of neutrophils and proinflammatory cytokines in schistosomal liver damage, we analyzed the mechanisms underlying neutrophil and proinflammatory responses in murine schistosomiasis japonica. We found that granulomatous inflammation around parasite eggs in the liver was greater in Schistosoma japonicum-infected IL-4?/? IL-13?/? (double-knockout [DKO]) mice than in infected wild-type (WT) mice at 6 weeks, but not at 8 weeks, postinfection, suggesting the importance of Th2 responses in these typical hepatic lesions. Infected DKO mice also showed increased neutrophil infiltration accompanying more severe pathology, as shown by the enhanced necrosis of hepatocytes. This was not likely due to a Th1/Th2 imbalance, because there was no detectable increase in gamma interferon (IFN-γ) production in these DKO mice. mRNA expression of interleukin-17A (IL-17A), proinflammatory cytokines, and the neutrophil chemoattractant CXCL2 in liver was higher in infected DKO mice than in WT mice. However, in IL-4?/? IL-13?/? IL-17A?/? (triple-knockout [TKO]) mice, the absence of IL-17A was associated with only marginal differences in schistosomal liver damage, suggesting that IL-17A is only partially responsible for neutrophil-driven hepatic damage. Furthermore, the expression of mRNAs encoding proinflammatory cytokines was not under the control of IL-17A in TKO mice. These findings indicate that IL-4 and IL-13 suppress excessive neutrophil recruitment, proinflammatory cytokine production, and hepatic damage during the acute stage of S. japonicum infection, suggesting that neutrophils and proinflammatory cytokines are mainly responsible for hepatocyte damage during acute murine schistosomiasis japonica. However, neutrophil induction and the production of proinflammatory cytokines were not due solely to IL-17A.
机译：由于嗜中性粒细胞和促炎细胞因子在血吸虫肝损害中的重要性，我们分析了日本血吸虫病中嗜中性粒细胞和促炎反应的潜在机制。我们发现在日本血吸虫感染的IL-4β/β中，肝脏中寄生虫卵周围的肉芽肿性炎症更大。 IL-13？/？ （双重敲除[DKO]）小鼠在感染后6周而不是8周时比感染的野生型（WT）小鼠要好，这表明Th2反应在这些典型的肝脏病变中的重要性。感染的DKO小鼠还显示出中性粒细胞浸润增加，伴有更严重的病理，这表现为肝细胞坏死增强。这不可能归因于Th1 / Th2失衡，因为在这些DKO小鼠中没有发现γ干扰素（IFN-γ）产生的增加。感染的DKO小鼠肝脏中白细胞介素17A（IL-17A），促炎细胞因子和嗜中性粒细胞趋化因子CXCL2的mRNA表达高于野生型小鼠。但是，在IL-4中？ IL-13？/？ IL-17A？/？ （三重敲除[TKO]）小鼠中，IL-17A的缺失仅与血吸虫肝损伤的边缘差异有关，这表明IL-17A仅部分负责中性粒细胞驱动的肝损伤。此外，在TKO小鼠中，编码促炎细胞因子的mRNA的表达不受IL-17A的控制。这些发现表明IL-4和IL-13在日本血吸虫感染的急性期抑制了过度的中性粒细胞募集，促炎性细胞因子的产生和肝损害，这表明中性粒细胞和促炎性细胞因子主要是造成急性鼠源性日本血吸虫病期间肝细胞损伤的原因。 。然而，嗜中性粒细胞的诱导和促炎细胞因子的产生并非仅由IL-17A引起。

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