Foster Neil, Tang Ying, Berchieri Angelo, Geng Shizhong, Jiao Xinan, Barrow Paul
SRUC Aberdeen Campus, Craibstone Estate, Ferguson Building, Aberdeen AB21 9YA, UK.
Institute of Molecular Physiology, Shenzhen Bay Laboratory, Shenzhen 518055, China.
Pathogens. 2021 Oct 9;10(10):1299. doi: 10.3390/pathogens10101299.
One characteristic of the few serovars that produce typhoid-like infections is that disease-free persistent infection can occur for months or years in a small number of individuals post-convalescence. The bacteria continue to be shed intermittently which is a key component of the epidemiology of these infections. Persistent chronic infection occurs despite high levels of circulating specific IgG. We have reviewed the information on the basis for persistence in . Typhi, . Dublin, Gallinarum, . Pullorum, . Abortusovis and also . Typhimurium in mice as a model of persistence. Persistence appears to occur in macrophages in the spleen and liver with shedding either from the gall bladder and gut or the reproductive tract. The involvement of host genetic background in defining persistence is clear from studies with the mouse but less so with human and poultry infections. There is increasing evidence that the organisms (i) modulate the host response away from the typical Th1-type response normally associated with immune clearance of an acute infection to Th2-type or an anti-inflammatory response, and that (ii) the bacteria modulate transformation of macrophage from M1 to M2 type. The bacterial factors involved in this are not yet fully understood. There are early indications that it might be possible to remodulate the response back towards a Th1 response by using cytokine therapy.
少数能引起伤寒样感染的血清型的一个特征是,在少数个体康复后,无病的持续性感染可持续数月或数年。细菌会持续间歇性排出,这是这些感染流行病学的一个关键因素。尽管循环中的特异性IgG水平很高,但仍会发生持续性慢性感染。我们已根据有关伤寒杆菌、都柏林沙门氏菌、鸡沙门氏菌、鸡白痢沙门氏菌、羊流产沙门氏菌以及作为持续性感染模型的鼠伤寒沙门氏菌持续性的相关信息进行了综述。持续性感染似乎发生在脾脏和肝脏的巨噬细胞中,细菌通过胆囊、肠道或生殖道排出。从小鼠研究中可以清楚地看出宿主遗传背景在决定持续性感染方面的作用,但在人类和家禽感染中作用较小。越来越多的证据表明,这些微生物(i)将宿主反应从通常与急性感染免疫清除相关的典型Th1型反应调节为Th2型反应或抗炎反应,并且(ii)细菌调节巨噬细胞从M1型向M2型的转变。其中涉及的细菌因素尚未完全了解。有早期迹象表明,通过使用细胞因子疗法,有可能将反应重新调节回Th1反应。