BACKGROUND NLRP12 has been shown to play an essential role as a negative regulator in several bacterial infection. OBJECTIVE The purpose of this study is to elucidate the role of NLRP12 in B. pseudomallei-infected RAW264.7 macrophages. METHODS The protein expression and the level of TNF-α production were determined by immunoblotting and ELISA assay, respectively. RESULTS The results demonstrated that unlike the LPS-mutant strain which lacks O antigenic polysaccharide, the wild-type B. pseudomallei was able to upregulate NLRP12 protein expression in RAW264.7 macrophages. NLRP12 expression also correlated with the suppression of TNF-α production as demonstrated in wild-type B. pseudomallei-infected Nlrp12-depleted macrophages when compared to that of the control siRNA-transfected cells. The expression of NLRP12 was also inhibited in cytochalasin D treated cells. CONCLUSIONS Our findings showed that wild-type B. pseudomallei can activate NLRP12 expression leading to the suppression of TNF-α production. It is possible that the regulation of NLRP12 may contribute to the pathogenesis of B. pseudomallei infection in melioidosis patients.

中文翻译：

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NLRP12 减弱被假槌氏菌感染的 RAW264.7 巨噬细胞中肿瘤坏死因子-α 的产生。

背景 NLRP12 已被证明在几种细菌感染中作为负调节剂发挥重要作用。目的本研究的目的是阐明NLRP12 在B. pseudomallei 感染的RAW264.7 巨噬细胞中的作用。方法通过免疫印迹法和ELISA法分别测定蛋白表达和TNF-α产生水平。结果结果表明，与缺乏O抗原多糖的LPS突变株不同，野生型B. pseudomallei能够上调RAW264.7巨噬细胞中NLRP12蛋白的表达。与对照 siRNA 转染的细胞相比，NLRP12 表达也与抑制 TNF-α 产生相关，如野生型 B. pseudomallei 感染的 Nlrp12 耗尽的巨噬细胞中所证明的那样。NLRP12 的表达在细胞松弛素 D 处理的细胞中也受到抑制。结论 我们的研究结果表明，野生型 B. pseudomallei 可以激活 NLRP12 表达，从而抑制 TNF-α 的产生。NLRP12 的调节可能有助于类鼻疽患者感染 B. pseudomallei 的发病机制。