Tracheitis associated with the chronic respiratory disease in chickens caused by Mycoplasma gallisepticum is marked by infiltration of leukocytes into the mucosa. Although cytokines/chemokines are known to play a key role in the recruitment, differentiation, and proliferation of leukocytes, those that are produced and secreted into the trachea during the chronic stages of infection with M. gallisepticum have not been described previously. In this study, the levels of transcription in the trachea of genes encoding a panel of 13 cytokines/chemokines were quantified after experimental infection with the M. gallisepticum wild-type strain Ap3AS in unvaccinated chickens and chickens vaccinated 40-, 48- or 57-weeks previously with the novel attenuated strain ts-304. These transcriptional levels in unvaccinated/infected and vaccinated/infected chickens were compared with those of unvaccinated/uninfected and vaccinated/uninfected chickens. Pathological changes and subsets of leukocytes infiltrating the tracheal mucosa were concurrently assessed by histopathological examination and indirect immunofluorescent staining. After infection, unvaccinated birds had a significant increase in tracheal mucosal thickness and in transcription of genes for cytokines/chemokines, including those for IFN-γ, IL-17, RANTES (CCLi4), and CXCL-14, and significant downregulation of IL-2 gene transcription. B cells, CD3⁺ or CD4⁺ cells and macrophages (KUL01⁺) accumulated in the mucosa but CD8⁺ cells were not detected. In vaccinated birds, the levels of transcription of the genes for IL-6, IL-2, RANTES and CXCL-14 were significantly lower after infection than in the unvaccinated/infected and/or unvaccinated/uninfected birds, while the transcription of the IFN-γ gene was significantly upregulated, and there were aggregations of B cells in the tracheal mucosa. These observations indicated that M. gallisepticum may have suppressed Th2 responses by upregulating secretion of IFN-γ and IL-17 by CD4⁺ cells and induced immune dysregulation characterized by depletion of CD8⁺ cells and downregulation of IL-2 in the tracheas of unvaccinated birds. The ts-304 vaccine appeared to induce long-term protection against this immune dysregulation.

中文翻译：

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未接种和接种过疫苗的成熟鸡慢性感染鸡毒支原体后气管黏膜免疫反应

鸡感染支原体引起的与鸡慢性呼吸道疾病相关的气管炎的特点是白细胞浸润到黏膜中。尽管已知细胞因子/趋化因子在白细胞的募集、分化和增殖中起关键作用，但在鸡毒支原体感染的慢性阶段产生并分泌到气管中的那些细胞因子/趋化因子以前没有被描述过。在这项研究中，在用鸡毒支原体进行实验性感染后，量化了编码一组 13 种细胞因子/趋化因子的基因在气管中的转录水平在未接种疫苗的鸡和 40、48 或 57 周前用新型减毒菌株 ts-304 接种的鸡中发现野生型菌株 Ap3AS。将未接种疫苗/感染和接种疫苗/感染鸡的这些转录水平与未接种疫苗/未感染和接种疫苗/未感染鸡的转录水平进行比较。通过组织病理学检查和间接免疫荧光染色同时评估浸润气管粘膜的白细胞的病理变化和亚群。感染后，未接种疫苗的禽类气管黏膜厚度和细胞因子/趋化因子基因转录显着增加，包括 IFN-γ、IL-17、RANTES (CCLi4) 和 CXCL-14 基因的转录，以及显着下调 IL- 2基因转录。B 细胞，CD3 ⁺或 CD4 ⁺细胞和巨噬细胞 (KUL01 ⁺ ) 在黏膜中积累，但未检测到 CD8 ⁺细胞。在接种疫苗的鸟类中，感染后 IL-6、IL-2、RANTES 和 CXCL-14 基因的转录水平显着低于未接种疫苗/感染和/或未接种疫苗/未感染的鸟类，而 IFN 的转录水平显着降低。 -γ基因显着上调，气管黏膜有B细胞聚集。这些观察结果表明，鸡毒支原体可能通过上调 CD4 ^{+细胞分泌 IFN-γ 和 IL-17 并诱导以 CD8 +}耗竭为特征的免疫失调来抑制 Th2 反应。未接种疫苗的鸟类气管中细胞和 IL-2 的下调。ts-304 疫苗似乎诱导针对这种免疫失调的长期保护。