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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Critical Role of IL-22/IL22-RA1 Signaling in Pneumococcal Pneumonia
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Critical Role of IL-22/IL22-RA1 Signaling in Pneumococcal Pneumonia

机译：IL-22 / IL22-RA1信号在肺炎球菌肺炎中的关键作用

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摘要

IL-22-IL-22R signaling plays a crucial role in regulating host defenses against extracellular pathogens, particularly in the intestine, through the induction of antimicrobial peptides and chemotactic genes. However, the role of IL-22-IL-22R is understudied in Streptococcus pneumoniae lung infection, a prevalent pathogen of pneumonia. This paper presents the findings of IL-22 signaling during a murine model of pneumococcal pneumonia and improvement of bacterial burden upon IL-22 administration. IL-22 was rapidly induced in the lung during pneumococcal infection in wild-type mice, and Il22(-/-) mice had higher pneumococcal burdens compared with controls. Additionally, mice with hepatic-specific deletion of Il22ra1 also had higher bacterial burdens in lungs compared with littermate controls after intrapulmonary pneumococcal infection, suggesting that IL-22 signaling in the liver is important to control pneumococcal pneumonia. Thus, we hypothesized that enhancement of IL-22 signaling would control pneumococcal burden in lung tissues in an experimental pneumonia model. Administration of rIL-22 systemically to infected wild-type mice decreased bacterial burden in lung and liver at 24 h postinfection. Our in vitro studies also showed that mice treated with IL-22 had increased C3 expression in the liver compared with the isotype control group. Furthermore, serum from mice treated with IL-22 had improved opsonic capacity by increasing C3 binding on S. pneumoniae. Taken together, endogenous IL-22 and hepatic IL-22R signaling play critical roles in controlling pneumococcal lung burden, and systemic IL-22 decreases bacterial burden in the lungs and peripheral organs by potentiating C3 opsonization on bacterial surfaces, through the increase of hepatic C3 expression.
机译：IL-22-IL-22R信号传导在调节针对细胞外病原体的宿主防御，特别是在肠道，通过诱导抗微生物肽和趋化基因来发挥至关重要的作用。然而，IL-22-IL-22R的作用在肺炎链球菌肺部感染中被肺炎链球菌肺部感染，是肺炎普遍的病原体。本文介绍了在肺炎球菌肺炎的小鼠模型中的IL-22信号传导的结果，并在IL-22给药时改善细菌负担。在野生型小鼠的肺炎球菌感染期间，在肺炎球菌期间迅速诱导IL-22，与对照组相比，IL22（ - / - ）小鼠具有更高的肺炎球菌负担。另外，与患有IL22A11的肝细胞特异性缺失的小鼠在肺内肺炎球菌感染后与凋落物相比，肺部的细菌负担较高，表明IL-22在肝脏中的信号传导对控制肺炎球菌肺炎是重要的。因此，我们假设IL-22信号传导的增强将控制实验性肺炎模型中肺组织的肺炎球菌负担。系统性地施用于Ril-22，感染野生型小鼠降低了24小时的肺癌和肝脏的细菌负担。我们的体外研究还表明，与同种型对照组相比，用IL-22处理的小鼠在肝脏中增加了C3表达。此外，通过增加肺炎肺炎的C3结合，通过IL-22处理的小鼠来自小鼠的血清。在一起，内源性IL-22和肝脏IL-22R信号传导在控制肺炎球菌肺负担方面发挥关键作用，通过增加肝C3的细菌表面上增强C3 OPSON化，通过增强C3 OPSON化来降低肺部和外周器官的细菌负荷。表达。

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