Background

Mycoplasma ovipneumoniae (M. ovi) is the causative agent of chronic non-progressive pneumonia in sheep, goats, bighorn, and wild small ruminants. However, the mechanism of infection and immune response to M. ovi remain unclear. Invading microbes express lipid-associated membrane proteins (LAMPs) on the cell surface that interact with host cells to facilitate infection, and are thus the major molecules recognised by the host immune system. Upon LAMP recognition, Toll-like receptor 2 (TLR2) and NLRP3 inflammasome sense the pathogens and signalling pathways for cytokine secretion. In this study, we investigated whether M. ovi and M. ovi-derived LAMPs are immuno-biologically active compounds capable of activating mouse peritoneal macrophages and explored the underlying mechanism.

Results

After infection of wild-type mice with M. ovi, the expression of TLR2 and NLRP3 at the transcriptional and translational levels was determined with reverse transcription-polymerase chain reaction and flow cytometry. In addition, the cytokine levels and associated pathways were detected in infected wild-type, Tlr2^−/−, and Nlrp3^−/− mice via enzyme-linked immunosorbent assays and western blotting. The nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signalling pathways were found to mediate the expression of inflammatory cytokines in M. ovi or M. ovi-derived LAMP-infected peritoneal macrophages, and cytokines were not induced in Tlr2^−/− and/or Nlrp3^−/− macrophages.

Conclusion

Host cytokine production is activated in response to M. ovi-derived LAMPs through the NF-κB and MAPK signalling pathway via TLR2.

中文翻译：

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猪肺炎支原体来源的脂质相关膜蛋白通过TLR2信号传导诱导小鼠腹膜巨噬细胞分泌细胞因子。

背景

猪肺炎支原体（M. ovi）是绵羊，山羊，大角羊和野生小反刍动物中慢性非进行性肺炎的病原体。但是，感染的机制和对卵母鼠的免疫应答仍然不清楚。入侵的微生物在细胞表面表达与宿主细胞相互作用以促进感染的脂质相关膜蛋白（LAMP），因此是宿主免疫系统识别的主要分子。LAMP识别后，Toll样受体2（TLR2）和NLRP3炎性小体检测到病原体和细胞因子分泌的信号通路。在这项研究中，我们调查了M. ovi和M. ovi衍生的LAMP是能够激活小鼠腹膜巨噬细胞的免疫生物活性化合物，并探索了其潜在机制。

结果

与野生型小鼠的感染后M.的Ovi，用反转录-聚合酶链反应和流式细胞术确定TLR2和NLRP3的在转录和翻译水平的表达。另外，通过酶联免疫吸附测定和蛋白质印迹，在感染的野生型，Tlr2 ^-/-和Nlrp3 ^-//-小鼠中检测到细胞因子水平和相关途径。发现核因子（NF）-κB和有丝分裂原激活的蛋白激酶（MAPK）信号通路介导了M. ovi或M. ovi派生的LAMP感染的腹膜巨噬细胞中炎性细胞因子的表达，而在Tlr2 ^-/-和/或Nlrp3 ^-/-巨噬细胞。

结论

响应TLV，通过TLR2通过NF-κB和MAPK信号通路激活宿主细胞因子。