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Functional CD40 Expression Induced following Bacterial Infection of Mouse and Human Osteoblasts

机译：小鼠和人类成骨细胞细菌感染后诱导功能性CD40表达。

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Bacterially induced bone infections often result in significant local inflammatory responses which are coupled with loss of bone. However, the mechanisms necessary for the protective host response, or those responsible for pathogen-induced bone loss, are not clear. Recent evidence demonstrates that bacterially infected osteoblasts secrete chemokines and cytokines, suggesting that these cells may have an unappreciated role in supporting localized inflammation. In this study, mouse and human osteoblasts were investigated for their ability to express functional CD40 upon exposure to two important pathogens of bone, Staphylococcus aureus and Salmonella enterica serovar Dublin. Bacterial infection of cultured mouse or human osteoblasts resulted in increased CD40 mRNA and CD40 protein expression induced by either pathogen. Importantly, CD40 expression by osteoblasts was functional, as assessed by ligation of this molecule with recombinant, soluble CD154. CD40 activity was assessed by induction of interleukin-6 and granulocyte-macrophage colony-stimulating factor in osteoblasts following ligation. Cocultures of activated CD4+ T lymphocytes and osteoblasts could interact via CD40 and CD154, since an antibody against CD40 could block macrophage inflammatory protein-1α secretion. Taken together, these studies conclusively demonstrate that infected osteoblasts can upregulate expression of functional CD40 molecules which mediate cytokine secretion. This surprising result further supports the notion that bone-forming osteoblasts can directly interact with CD154-expressing cells (i.e., T lymphocytes) and can contribute to the host response during bone infection.
机译：细菌引起的骨感染通常会导致明显的局部炎症反应，并伴有骨质流失。但是，对于保护性宿主反应或负责病原体引起的骨丢失的机制尚不清楚。最近的证据表明，细菌感染的成骨细胞分泌趋化因子和细胞因子，表明这些细胞在支持局部炎症中的作用可能不明显。在这项研究中，研究了小鼠和人类成骨细胞在暴露于两种重要骨病原体金黄色葡萄球菌和肠沙门氏菌血清都柏林后表达功能性CD40的能力。培养的小鼠或人成骨细胞的细菌感染导致由任一病原体诱导的CD40 mRNA和CD40蛋白表达增加。重要的是，通过将该分子与重组的可溶性CD154连接评估，成骨细胞表达CD40是功能性的。连接后通过诱导白细胞介素6和粒细胞巨噬细胞集落刺激因子诱导CD40活性。活化的CD4 + T淋巴细胞与成骨细胞的共培养可以通过CD40和CD154相互作用，因为抗CD40的抗体可以阻止巨噬细胞炎性蛋白1α的分泌。综上所述，这些研究最终证明受感染的成骨细胞可以上调介导细胞因子分泌的功能性CD40分子的表达。这一令人惊讶的结果进一步支持了以下观点：成骨成骨细胞可以直接与表达CD154的细胞（即T淋巴细胞）相互作用，并且可以在骨感染期间促进宿主反应。

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