Faulkner C B, Simecka J W, Davidson M K, Davis J K, Schoeb T R, Lindsey J R, Everson M P
Department of Comparative Medicine, University of Alabama at Birmingham, USA.
Infect Immun. 1995 Oct;63(10):4084-90. doi: 10.1128/iai.63.10.4084-4090.1995.
Studies were conducted to determine whether the production of various cytokines is associated with Mycoplasma pulmonis disease expression. Susceptible C3H/HeN and resistant C57BL/6N mice were inoculated intranasally with 10(7) CFU of virulent M. pulmonis UAB CT or avirulent M. pulmonis UAB T. Expression of genes for tumor necrosis factor alpha (TNF-alpha), interleukin 1 alpha (IL-1 alpha), IL-1 beta, IL-6, and gamma interferon (IFN-gamma) in whole lung tissue and TNF-alpha gene expression in bronchoalveolar lavage (BAL) cells was determined by reverse transcription-PCR using specific cytokine primers at various times postinoculation. In addition, concentrations of TNF-alpha, IL-1, IL-6, and IFN-gamma were determined in BAL fluid and serum samples at various times postinoculation. Our results showed that there was a sequential appearance of cytokines in the lungs of infected mice: TNF-alpha, produced primarily by BAL cells, appeared first, followed by IL-1 and IL-6, which were followed by IFN-gamma. Susceptible C3H/HeN mice had higher and more persistent concentrations of TNF-alpha and IL-6 in BAL fluid than did resistant C57BL/6N mice, indicating that TNF-alpha and possibly IL-6 are important factors in pathogenesis of acute M. pulmonis disease in mice. Serum concentrations of IL-6 were elevated in C3H/HeN mice, but not C57BL/6N mice, following infection with M. pulmonis, suggesting that IL-6 has both local and systemic effects in M. pulmonis disease.
开展了多项研究以确定各种细胞因子的产生是否与肺支原体疾病的表现相关。将10(7)CFU的强毒肺支原体UAB CT或无毒肺支原体UAB T经鼻接种于易感的C3H/HeN小鼠和抗性的C57BL/6N小鼠。在接种后的不同时间,使用特异性细胞因子引物通过逆转录聚合酶链反应(RT-PCR)测定全肺组织中肿瘤坏死因子α(TNF-α)、白细胞介素1α(IL-1α)、IL-1β、IL-6和γ干扰素(IFN-γ)的基因表达以及支气管肺泡灌洗(BAL)细胞中TNF-α基因的表达。此外,在接种后的不同时间测定BAL液和血清样本中TNF-α、IL-1、IL-6和IFN-γ的浓度。我们的结果表明,感染小鼠的肺中细胞因子呈序贯出现:主要由BAL细胞产生的TNF-α首先出现,随后是IL-1和IL-6,接着是IFN-γ。易感的C3H/HeN小鼠BAL液中TNF-α和IL-6的浓度高于抗性的C57BL/6N小鼠且持续时间更长,这表明TNF-α以及可能的IL-6是小鼠急性肺支原体病发病机制中的重要因素。感染肺支原体后,C3H/HeN小鼠血清中IL-6浓度升高,但C57BL/6N小鼠未升高,这表明IL-6在肺支原体病中具有局部和全身作用。