Devi Vemuri Rama, Poumarat François, Le Grand Dominique, Rosengarten Renate, Hermeyer Kathrin, Hewicker-Trautwein Marion
Department of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, Hannover, D-30559, Germany.
Acta Vet Scand. 2014 Aug 19;56(1):45. doi: 10.1186/s13028-014-0045-3.
The pathogenesis of caseonecrotic lesions developing in lungs and joints of calves infected with Mycoplasma bovis is not clear and attempts to prevent M. bovis-induced disease by vaccines have been largely unsuccessful. In this investigation, joint samples from 4 calves, i.e. 2 vaccinated and 2 non-vaccinated, of a vaccination experiment with intraarticular challenge were examined. The aim was to characterize the histopathological findings, the phenotypes of inflammatory cells, the expression of class II major histocompatibility complex (MHC class II) molecules, and the expression of markers for nitritative stress, i.e. inducible nitric oxide synthase (iNOS) and nitrotyrosine (NT), in synovial membrane samples from these calves. Furthermore, the samples were examined for M. bovis antigens including variable surface protein (Vsp) antigens and M. bovis organisms by cultivation techniques.
The inoculated joints of all 4 calves had caseonecrotic and inflammatory lesions. Necrotic foci were demarcated by phagocytic cells, i.e. macrophages and neutrophilic granulocytes, and by T and B lymphocytes. The presence of M. bovis antigens in necrotic tissue lesions was associated with expression of iNOS and NT by macrophages. Only single macrophages demarcating the necrotic foci were positive for MHC class II. Microbiological results revealed that M. bovis had spread to approximately 27% of the non-inoculated joints. Differences in extent or severity between the lesions in samples from vaccinated and non-vaccinated animals were not seen.
The results suggest that nitritative injury, as in pneumonic lung tissue of M. bovis-infected calves, is involved in the development of caseonecrotic joint lesions. Only single macrophages were positive for MHC class II indicating down-regulation of antigen-presenting mechanisms possibly caused by local production of iNOS and NO by infiltrating macrophages.
感染牛支原体的犊牛肺部和关节中发生的干酪样坏死病变的发病机制尚不清楚，通过疫苗预防牛支原体引起的疾病的尝试大多未成功。在这项研究中，对一项关节内攻毒疫苗接种实验的4头犊牛（2头接种疫苗和2头未接种疫苗）的关节样本进行了检查。目的是对这些犊牛滑膜样本中的组织病理学发现、炎症细胞表型、II类主要组织相容性复合体（MHC II类）分子的表达以及亚硝化应激标志物（即诱导型一氧化氮合酶（iNOS）和硝基酪氨酸（NT））的表达进行表征。此外，通过培养技术对样本进行牛支原体抗原检测，包括可变表面蛋白（Vsp）抗原和牛支原体菌体。
所有4头犊牛接种的关节均有干酪样坏死和炎症病变。坏死灶由吞噬细胞（即巨噬细胞和嗜中性粒细胞）以及T和B淋巴细胞界定。坏死组织病变中牛支原体抗原的存在与巨噬细胞中iNOS和NT的表达相关。仅界定坏死灶的单个巨噬细胞MHC II类呈阳性。微生物学结果显示，牛支原体已扩散至约27%未接种的关节。未观察到接种和未接种动物样本中病变在范围或严重程度上的差异。
结果表明，如牛支原体感染犊牛的肺组织一样，亚硝化损伤参与了干酪样坏死性关节病变的发展。仅单个巨噬细胞MHC II类呈阳性，表明抗原呈递机制下调，这可能是由浸润的巨噬细胞局部产生iNOS和NO所致。
