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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Interleukin-10 plays a key role in the modulation of neutrophils recruitment and lung inflammation during infection by Streptococcus pneumoniae
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Interleukin-10 plays a key role in the modulation of neutrophils recruitment and lung inflammation during infection by Streptococcus pneumoniae

机译：白细胞介素10在肺炎链球菌感染期间中性粒细胞募集和肺部炎症的调节中起关键作用

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摘要

Streptococcus pneumoniae is a major aetiological agent of pneumonia worldwide, as well as otitis media, sinusitis, meningitis and sepsis. Recent reports have suggested that inflammation of lungs due to S.pneumoniae infection promotes bacterial dissemination and severe disease. However, the contribution of anti-inflammatory molecules to the pathogenesis of S.pneumoniae remains unknown. To elucidate whether the production of the anti-inflammatory cytokine interleukin-10 (IL-10) is beneficial or detrimental for the host during pneumococcal pneumonia, we performed S.pneumoniae infections in mice lacking IL-10 (IL-10(-/-) mice). The IL-10(-/-) mice showed increased mortality, higher expression of pro-inflammatory cytokines, and an exacerbated recruitment of neutrophils into the lungs after S.pneumoniae infection. However, IL-10(-/-) mice showed significantly lower bacterial loads in lungs, spleen, brain and blood, when compared with mice that produced this cytokine. Our results support the notion that production of IL-10 during S.pneumoniae infection modulates the expression of pro-inflammatory cytokines and the infiltration of neutrophils into the lungs. This feature of IL-10 is important to avoid excessive inflammation of tissues and to improve host survival, even though bacterial dissemination is less efficient in the absence of this cytokine.
机译：肺炎链球菌是全世界范围内肺炎以及中耳炎，鼻窦炎，脑膜炎和败血症的主要病因。最近的报道表明，由于肺炎链球菌感染引起的肺部炎症促进细菌传播和严重疾病。然而，抗炎分子对肺炎链球菌的发病机理的贡献仍然未知。为了阐明在肺炎球菌性肺炎期间抗炎细胞因子白介素10（IL-10）的产生对宿主是有益还是有害，我们在缺乏IL-10的小鼠中进行了肺炎链球菌感染（IL-10（-/- ） 老鼠）。 IL-10（-/-）小鼠在肺炎链球菌感染后显示出更高的死亡率，促炎性细胞因子更高的表达以及嗜中性粒细胞向肺的募集加剧。但是，与产生这种细胞因子的小鼠相比，IL-10（-/-）小鼠在肺，脾脏，大脑和血液中的细菌负荷显着降低。我们的结果支持以下观念：在肺炎链球菌感染过程中产生IL-10会调节促炎性细胞因子的表达以及中性粒细胞向肺的浸润。 IL-10的这一特征对于避免组织过度炎症和提高宿主存活率非常重要，即使在缺乏这种细胞因子的情况下细菌传播的效率较低。

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