Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, PO Box 100136, Gainesville, FL 32610, USA.
Department of Veterinary and Biomedical Sciences, South Dakota State University, PO Box 2175, SAR Room 125 North Campus Drive, Brookings, SD 57007, USA.
Vet Clin North Am Food Anim Pract. 2019 Nov;35(3):471-483. doi: 10.1016/j.cvfa.2019.08.003.
Host responses are often ineffective at clearing Mycoplasma bovis infection and may contribute to the pathogenesis of disease. M bovis possesses a surprisingly large repertoire of strategies to evade and modulate host responses. Unopsonized M bovis impairs phagocytosis and killing by neutrophils and macrophages. Apoptosis of neutrophils and lymphocytes is enhanced, whereas it is delayed in macrophages. Both proinflammatory and antiinflammatory cytokines are stimulated during M bovis infection depending on the cell type and location, and overall systemic responses tend to have a T-helper 2 bias. M bovis reduces proliferation of T cells and, in chronic infection, causes T-cell exhaustion.
宿主反应常常无法有效清除牛支原体感染,可能导致疾病的发生。牛支原体拥有令人惊讶的大量逃避和调节宿主反应的策略。非调理的牛支原体削弱了中性粒细胞和巨噬细胞的吞噬和杀伤作用。中性粒细胞和淋巴细胞的凋亡被增强,而巨噬细胞的凋亡则被延迟。在牛支原体感染过程中,根据细胞类型和位置,会刺激促炎和抗炎细胞因子,并且整体系统反应往往偏向辅助性 T 细胞 2 型(T-helper 2 bias)。牛支原体降低 T 细胞的增殖,在慢性感染中导致 T 细胞衰竭。