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首页> 外文期刊>Infection and immunity >Roles of autolysin and pneumolysin in middle ear inflammation caused by a type 3 Streptococcus pneumoniae strain in the chinchilla otitis media model.
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Roles of autolysin and pneumolysin in middle ear inflammation caused by a type 3 Streptococcus pneumoniae strain in the chinchilla otitis media model.

机译：自溶素和肺炎球菌溶血素在黄鼠中耳炎模型中由3型肺炎链球菌菌株引起的中耳炎症中的作用。

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摘要

Streptococcus pneumoniae cell wall and pneumolysin are important contributors to pneumococcal pathogenicity in some animal models. To further explore these factors in middle ear inflammation caused by pneumococci, penicillin-induced inflammatory acceleration was studied by using three closely related pneumococcal strains: a wild-type 3 strain (WT3), its pneumolysin-negative derivative (P-1), and into autolysin-negative derivative (A-1). Both middle ears of chinchillas were inoculated with one of the three pneumococcal strains. During the first 12 h, all three strains grew in vivo at the same rate, and all three strains induced similar inflammatory cell responses in middle ear fluid (MEF). Procaine penicillin G was given as 12 h to one-half of the animals in each group, and all treated chinchillas had sterile MEF at 24 h. Penicillin significantly accelerated MEF inflammatory cell influx into WT3-and P-1-infected ears at 18 and 24 h in comparison with the rate for penicillin-treated A-1-infected ears. Inflammatory cell influx was slightly, but not significantly, greater after treatment of WT3 infection than after treatment of P-1 infection. Interleukin (IL)-1beta and IL-6, but not IL-8, concentrations in MEF at 24 h reflected the penicillin effect on MEF inflammatory cells; however, differences between treatment groups were not significant. Results suggest that pneumococcal otitis media pathogenesis is triggered principally by the inflammatory effects of intact and lytic cell wall products in the middle ear, with at most a modes additional pneumolysin effect. Investigation strategies that limit the release of these products or neutralize them warrant further investigation.
机译：在某些动物模型中，肺炎链球菌的细胞壁和肺炎球菌溶血素是导致肺炎球菌致病性的重要因素。为了进一步探讨由肺炎球菌引起的中耳炎症中的这些因素，我们使用三种密切相关的肺炎球菌菌株研究了青霉素诱导的炎症促进作用：野生型3株（WT3），其肺炎球菌溶血素阴性衍生物（P-1）和成自溶素阴性衍生物（A-1）。用三种肺炎球菌菌株之一接种龙猫的两个中耳。在最初的12小时内，所有三个菌株在体内的生长速率均相同，并且所有三个菌株在中耳液（MEF）中诱导相似的炎症细胞反应。每组一半的动物在12小时内给予普鲁卡因青霉素G，所有治疗的龙猫在24 h均具有无菌MEF。与青霉素治疗的A-1感染的耳朵相比，青霉素在18和24 h显着加速了MEF炎性细胞向WT3和P-1感染的耳朵的流入。治疗WT3感染后，炎性细胞流入量略大于但不明显，而治疗P-1感染后则更大。白细胞介素（IL）-1beta和IL-6，而不是IL-8，在24 h时的浓度反映了青霉素对MEF炎性细胞的作用。然而，治疗组之间的差异并不显着。结果表明，肺炎球菌性中耳炎的发病机理主要是由中耳完整和溶解性细胞壁产物的炎症作用触发的，至多有一种其他的肺炎球菌溶血素作用。限制这些产品释放或中和它们的调查策略值得进一步调查。

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