首页> 外文期刊>Infection and immunity >Elevated Cytokine and Chemokine Levels and Prolonged Pulmonary Airflow Resistance in a Murine Mycoplasma pneumoniaePneumonia Model: a Microbiologic, Histologic, Immunologic, and Respiratory Plethysmographic Profile
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Elevated Cytokine and Chemokine Levels and Prolonged Pulmonary Airflow Resistance in a Murine Mycoplasma pneumoniaePneumonia Model: a Microbiologic, Histologic, Immunologic, and Respiratory Plethysmographic Profile

机译:小鼠肺炎支原体肺炎模型中细胞因子和趋化因子水平升高以及肺通气阻力延长:微生物学,组织学,免疫学和呼吸道呼吸描记谱

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Because Mycoplasma pneumoniae is hypothesized to play an important role in reactive airway disease/asthma, a comprehensive murine model of M. pneumoniae lower respiratory infection was established. BALB/c mice were intranasally inoculated once withM. pneumoniae and sacrificed at 0 to 42 days postinoculation. All mice became infected and developed histologic evidence of acute pulmonary inflammation, which cleared by 28 days postinoculation. By contrast, M. pneumoniae persisted in the respiratory tract for the entire 42 days studied. Tumor necrosis factor alpha, gamma interferon, interleukin-6 (IL-6), KC (functional IL-8), MIP-1α, and MCP-1/JE concentrations were significantly elevated in bronchoalveolar lavage samples, whereas IL-4 and IL-10 concentrations were not significantly elevated. Pulmonary airflow resistance, as measured by plethysmography, was detected 1 day postinoculation and persisted even after pulmonary inflammation had resolved at day 28. Serum anti-M. pneumoniae immunoglobulin G titers were positive in all mice by 35 days. This mouse model provides a means to investigate the immunopathogenesis of M. pneumoniae infection and its possible role in reactive airway disease/asthma.
机译:由于假设肺炎支原体在反应性气道疾病/哮喘中起重要作用,因此 M的综合性小鼠模型。建立了肺炎下呼吸道感染。将BALB / c小鼠鼻内接种em。肺炎并在接种后0至42天处死。所有小鼠均被感染并发展为急性肺部炎症的组织学证据,接种后28天即可清除。相比之下, M。在研究的整整42天中,肺炎持续存在于呼吸道中。支气管肺泡灌洗样品中的肿瘤坏死因子α,γ干扰素,白介素6(IL-6),KC(功能性IL-8),MIP-1α和MCP-1 / JE浓度显着升高,而IL-4和IL -10浓度没有明显升高。接种1天后检测出通过体积描记法测得的肺气流阻力,即使在第28天肺部炎症消退后,肺气流阻力仍持续存在。血清抗 M。到第35天,所有小鼠的肺炎球菌免疫球蛋白G滴度均呈阳性。该小鼠模型提供了研究 M的免疫发病机制的手段。肺炎感染及其在反应性气道疾病/哮喘中的可能作用。

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