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首页> 外文期刊>Infection and immunity >Induction of Nod1 and Nod2 Intracellular Pattern Recognition Receptors in Murine Osteoblasts following Bacterial Challenge
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Induction of Nod1 and Nod2 Intracellular Pattern Recognition Receptors in Murine Osteoblasts following Bacterial Challenge

机译：细菌攻击后小鼠成骨细胞中Nod1和Nod2细胞内模式识别受体的诱导。

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Osteoblasts produce an array of immune molecules following bacterial challenge that could recruit leukocytes to sites of infection and promote inflammation during bone diseases, such as osteomyelitis. Recent studies from our laboratory have shed light on the mechanisms by which this cell type can perceive and respond to bacteria by demonstrating the functional expression of members of the Toll-like family of cell surface pattern recognition receptors by osteoblasts. However, we have shown that bacterial components fail to elicit immune responses comparable with those seen following challenge with the intracellular pathogens salmonellae and Staphylococcus aureus. In the present study, we show that UV-killed bacteria and invasion-defective bacterial strains elicit significantly less inflammatory cytokine production than their viable wild-type counterparts. Importantly, we demonstrate that murine osteoblasts express the novel intracellular pattern recognition receptors Nod1 and Nod2. Levels of mRNA encoding Nod molecules and protein expression are significantly and differentially increased from low basal levels following exposure to these disparate bacterial pathogens. In addition, we have shown that osteoblasts express Rip2 kinase, a critical downstream effector molecule for Nod signaling. Furthermore, to begin to establish the functional nature of Nod expression, we show that a specific ligand for Nod proteins can significantly augment immune molecule production by osteoblasts exposed to either UV-inactivated bacteria or bacterial lipopolysaccharide. As such, the presence of Nod proteins in osteoblasts could represent an important mechanism by which this cell type responds to intracellular bacterial pathogens of bone.
机译：成骨细胞在细菌攻击后产生一系列免疫分子，这些免疫分子可以将白细胞募集到感染部位，并在诸如骨髓炎的骨骼疾病中促进炎症。我们实验室的最新研究通过证明成骨细胞的Toll样细胞表面模式识别受体成员的功能性表达，揭示了这种细胞类型感知和响应细菌的机制。但是，我们已经证明，与细胞内病原体沙门氏菌和金黄色葡萄球菌攻击后相比，细菌成分无法引发免疫反应。在本研究中，我们表明，紫外线杀灭的细菌和侵袭性破坏的细菌菌株引起的炎性细胞因子的产生明显少于其野生型对应细菌。重要的是，我们证明了鼠成骨细胞表达新型细胞内模式识别受体Nod1和Nod2。暴露于这些不同的细菌病原体后，编码Nod分子和蛋白质表达的mRNA的水平与低基础水平相比有显着差异。此外，我们已经表明，成骨细胞表达Rip2激酶，这是Nod信号转导的关键下游效应分子。此外，为了开始建立Nod表达的功能性质，我们表明Nod蛋白的特异性配体可以显着增加暴露于紫外线灭活细菌或细菌脂多糖的成骨细胞的免疫分子产生。因此，成骨细胞中Nod蛋白的存在可能代表了一种重要的机制，通过这种机制，这种细胞类型可以对骨的细胞内细菌病原体做出反应。

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