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首页> 外文期刊>Infection and immunity >Role for Toll-Like Receptor 2 in the Immune Response to Streptococcus pneumoniae Infection in Mouse Otitis Media
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Role for Toll-Like Receptor 2 in the Immune Response to Streptococcus pneumoniae Infection in Mouse Otitis Media

机译：Toll样受体2在小鼠中耳炎对肺炎链球菌感染的免疫反应中的作用。

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Streptococcus pneumoniae is the most common pathogen associated with otitis media. To examine the role of Toll-like receptor 2 (TLR2) in host defense against Streptococcus pneumoniae infection in the middle ear, wild-type (WT; C57BL/6) and TLR2-deficient (TLR2?/?) mice were inoculated with Streptococcus pneumoniae (1 × 106 CFU) through the tympanic membrane. Nineteen of 37 TLR2?/? mice showed bacteremia and died within 3 days after the challenge, compared to only 4 of 32 WT mice that died. Of those that survived, more severe hearing loss in the TLR2?/? mice than in the WT mice was indicated by an elevation in auditory-evoked brain stem response thresholds at 3 or 7 days postinoculation. The histological pathology was characterized by effusion and tissue damage in the middle ear, and in the TLR2?/? mice, the outcome of infection became more severe at 7 days. At both 3 and 7 days postchallenge, the TLR2?/? mice had higher blood bacterial titers than the WT mice (P < 0.05), and typical bacteria were identified in the effusion from both ears of both mouse groups by acridine orange staining. Moreover, by 3 days postchallenge, the mRNA accumulation levels of NF-κB, tumor necrosis factor alpha, interleukin 1β, MIP1α, Muc5ac, and Muc5b were significantly lower in the ears of TLR2?/? mice than in WT mice. In summary, TLR2?/? mice may produce relatively low levels of proinflammatory cytokines following pneumococcal challenge, thus hindering the clearance of bacteria from the middle ear and leading to sepsis and a high mortality rate. This study provides evidence that TLR2 is important in the molecular pathogenesis and host response to otitis media.
机译：肺炎链球菌是与中耳炎相关的最常见病原体。目的探讨Toll样受体2（TLR2）在宿主抵抗中耳，野生型（WT; C57BL / 6）和TLR2缺陷型（TLR2 ？/？）小鼠通过鼓膜接种肺炎链球菌（1×10 6 CFU）。在攻击后的3天内，37只TLR2 α/β小鼠中有19只显示菌血症并死亡，而32只WT小鼠中只有4只死亡。在存活的那些小鼠中，接种后3或7天听觉诱发的脑干反应阈值升高表明，TLR2 α/β小鼠比WT小鼠更严重的听力丧失。组织病理学以中耳积液和组织损伤为特征，而在TLR2 ？/？小鼠中，感染的结果在第7天变得更加严重。攻击后第3天和第7天，TLR2 ？/？小鼠的血液细菌滴度比WT小鼠高（ P <0.05），并且在细菌中鉴定出典型细菌。通过mouse啶橙染色从两个小鼠组的两只耳朵流出。此外，攻击后3天，TLR2 ？/？小鼠的耳朵中NF-κB，肿瘤坏死因子α，白介素1β，MIP1α，Muc5ac和Muc5b的mRNA积累水平显着低于在野生型小鼠中。总之，在肺炎球菌攻击后，TLR2 α/β小鼠可能产生相对较低水平的促炎细胞因子，从而阻碍了细菌从中耳的清除并导致败血症和高死亡率。这项研究提供的证据表明，TLR2在分子发病机制和宿主对中耳炎的反应中很重要。

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