Esposito Susanna, Polinori Ilaria, Rigante Donato
Pediatric Clinic, Department of Surgical and Biomedical Sciences, Università degli Studi di Perugia, Perugia, Italy.
Institute of Pediatrics, IRCCS, Rome, Italy.
Front Pediatr. 2019 Apr 5;7:124. doi: 10.3389/fped.2019.00124. eCollection 2019.
Kawasaki syndrome (KS) is a necrotizing vasculitis of small- and medium-sized vessels mostly affecting children under 5 years of age; a host of clinical and epidemiological data supports the notion that KS might result from an infectious disease. However, many efforts have failed to identify a potentially universal trigger of KS. The contribution of the intestinal microbial community-called the "microbiota"-to KS has been evaluated by an increasing number of studies, though limited to small cohorts of patients. Differences in the microbiota composition were found in children with KS, both its acute and non-acute phase, with abnormal colonization by species in the intestinal tract and a wider presence of Gram-positive cocci in jejunal biopsies. In particular, a higher number of Gram-positive cocci (of the genera and ), , and HSP60-producing Gram-negative microbes have been found in the stools of KS children, and their effects on the antigenic repertoire of specific T cells and Vβ2 T cell expansion have been assessed. Conversely, were lacking in most children with KS compared with other febrile illnesses and healthy controls. All studies available to date have confirmed that an imbalance in the gut microbiota might indirectly interfere with the normal function of innate and adaptive immunity, and that variable microbiota interactions with environmental factors, mainly infectious agents, might selectively drive the development of KS in genetically susceptible children. Further investigations of the intestinal microflora in larger cohorts of KS patients will provide clues to disentangle the pathogenesis of this disease and probably indicate disease-modifying agents or more rational KS-specific therapies.
川崎病(KS)是一种主要影响5岁以下儿童的中小血管坏死性血管炎;大量临床和流行病学数据支持KS可能由传染病引起这一观点。然而,许多努力都未能确定KS潜在的普遍触发因素。越来越多的研究评估了肠道微生物群落(称为“微生物群”)对KS的影响,不过这些研究仅限于小样本患者队列。在KS患儿的急性期和非急性期均发现其微生物群组成存在差异,肠道中有物种异常定植,空肠活检中革兰氏阳性球菌的存在更为广泛。特别是,在KS患儿的粪便中发现了更多数量的革兰氏阳性球菌(属和属)、和产生热休克蛋白60的革兰氏阴性微生物,并评估了它们对特定T细胞抗原库和Vβ2 T细胞扩增的影响。相反,与其他发热性疾病和健康对照相比,大多数KS患儿缺乏。迄今为止所有可用研究均证实,肠道微生物群失衡可能间接干扰先天性和适应性免疫的正常功能,并且微生物群与环境因素(主要是感染因子)之间的可变相互作用可能在遗传易感儿童中选择性地推动KS的发展。对更大样本的KS患者队列中的肠道微生物群进行进一步研究,将为理清该疾病的发病机制提供线索,并可能指明疾病改善药物或更合理的KS特异性治疗方法。