背景:绵羊肺炎支原体(M.绵羊肺炎)是绵羊肺炎的主要病原体之一,引起一系列临床症状,比如抑郁症,厌食症,热疗,咳嗽,呼吸困难,和肠道分泌物。近年来,宁夏养羊场绵羊肺炎支原体肺炎的患病率日益严重,中国,导致羊的死亡,造成重大经济损失。在这项研究中,收集产卵肺炎支原体感染的病理器官,观察组织病理学改变,为了确定绵羊肺炎支原体的组织定位,并分析细胞因子的变化,为绵羊肺炎支原体病的诊断和发病机制奠定了基础。
结果:在这项研究中,通过PCR在从13个大型绵羊养殖场收集的105个样品中的97个中检测到绵羊肺炎支原体的核酸。从13个农场中分离出每个农场的一个代表性分离株。肺炎支原体引起的病变主要在气管,支气管,和肺,包括气管粘膜上皮细胞坏死,一些上皮细胞的解体,粘膜固有层水肿,炎性细胞浸润,支气管粘膜上皮细胞的细胞质空泡化,炎症细胞在肺的肺泡间隙大量浸润,肺泡上皮细胞坏死和增生。免疫组织化学分析显示肺组织中绵羊肺炎支原体阳性面积所占比例最大,其次是支气管和气管。与健康动物相比,患病动物表现出IL-1β基因表达水平上调,气管中的IL-6和NF-κB,支气管,还有肺.相比之下,IL-10,IL-12和IFN-γ的表达主要限于气管和支气管。IL-1β的表达在不同的肺区域显示出差异模式,在肺叶之间观察到变化。此外,其他细胞因子始终表现出明显的上调,特别是在支气管中。
结论:M.肺炎支原体主要存在于受感染个体的肺中。NF-κB,一种必需的转录因子,参与IL-1β转录的调节。IL-12可能在绵羊肺炎支原体感染期间增强自然杀伤细胞的细胞毒性功能。这些发现表明,在整个疾病进展过程中,细胞因子在各种解剖部位的不同表达谱。提示支气管组织作为免疫反应的主要部位的潜在作用。
BACKGROUND: Mycoplasma ovipneumoniae (M. ovipneumoniae) is one of the main pathogens of sheep pneumonia, causing a series of clinical symptoms, such as depression, anorexia, hyperthermia, cough, dyspnea, and tract secretions. In recent years, the prevalence of M. ovipneumoniae pneumonia has become increasingly serious in sheep farms in Ningxia,
China, leading to the death of sheep, and causing significant economic losses. In this study, the pathological organs infected by M. ovipneumoniae were collected to observe histopathological change, to determine the tissue localization of M. ovipneumoniae, and to analyze the cytokine changes, which lays a basis for the diagnosis and pathogenesis of M. ovipneumoniae disease.
RESULTS: In this study, M. ovipneumoniae was detected in 97 of 105 samples collected from 13 large-scale sheep farms for nucleic acid by PCR. One representative isolate per farm was isolated from 13 farms. The lesions caused by M. ovipneumoniae were mainly in the trachea, bronchus, and lung, including necrosis of tracheal mucosal epithelial cells, disintegration of some epithelial cells, edema of mucosal lamina propria, with inflammatory cell infiltration, cytoplasmic vacuolization of epithelial cells of bronchial mucosa, massive infiltration of inflammatory cells in the alveolar space of lung, necrosis and hyperplasia of alveolar epithelial cells. Immunohistochemical analysis showed that the proportion of M. ovipneumoniae positive area in the lung was the largest, followed by that in the bronchus and trachea. Compared to healthy animals, diseased animals exhibited up-regulated gene expression levels of IL-1β, IL-6, and NF-κB in the trachea, bronchus, and lungs. In contrast, the expression of IL-10, IL-12, and IFN-γ was primarily limited to the trachea and bronchus. The expression of IL-1β showed differential patterns across different lung regions, with variations observed among lung lobes. Additionally, other cytokines consistently showed significant up-regulation specifically in the bronchus.
CONCLUSIONS: M. ovipneumoniae is primarily found in the lungs of infected individuals. NF-κB, an essential transcription factor, is involved in the regulation of IL-1β transcription. IL-12 may enhance the cytotoxic function of natural killer cells during M. ovipneumoniae infection. Those findings demonstrate the distinct expression profiles of cytokines in various anatomical sites throughout disease progression, suggesting the potential role of bronchial tissue as a major site of immune response.