Picchianti-Diamanti Andrea, Rosado Maria M, D'Amelio Raffaele
Department of Clinical and Molecular Medicine, Sant'Andrea University Hospital, Sapienza University of Rome, Rome, Italy.
Independent Researcher, Rome, Italy.
Front Microbiol. 2018 Jan 16;8:2696. doi: 10.3389/fmicb.2017.02696. eCollection 2017.
In higher vertebrates, mucosal sites at the border between the internal and external environments, directly interact with bacteria, viruses, and fungi. Through co-evolution, hosts developed mechanisms of tolerance or ignorance toward some infectious agents, because hosts established "gain of function" interactions with symbiotic bacteria. Indeed, some bacteria assist hosts in different functions, among which are digestion of complex carbohydrates, and absorption and supply of vitamins. There is no doubt that microbiota modulate innate and acquired immune responses starting at birth. However, variations in quality and quantity of bacterial species interfere with the equilibrium between inflammation and tolerance. In fact, correlations between gut bacteria composition and the severity of inflammation were first described for inflammatory bowel diseases and later extended to other pathologies. The genetic background, environmental factors (e.g., stress or smoking), and diet can induce strong changes in the resident bacteria which can expose the intestinal epithelium to a variety of different metabolites, many of which have unknown functions and consequences. In addition, alterations in gut permeability may allow pathogens entry, thereby triggering infection and/or chronic inflammation. In this context, a local event occurring at a mucosal site may be the triggering cause of an autoimmune reaction that eventually involves distant sites or organs. Recently, several studies attributed a pathogenic role to altered oral microbiota in rheumatoid arthritis (RA) and to gut dysbiosis in spondyloarthritis (SpA). There is also growing evidence that different drugs, such as antibiotics and immunosuppressants, can influence and be influenced by the diversity and composition of microbiota in RA and SpA patients. Hence, in complex disorders such RA and SpA, not only the genetic background, gender, and immunologic context of the individual are relevant, but also the history of infections and the structure of the microbial community at mucosal sites should be considered. Here the role of the microbiota and infections in the initiation and progression of chronic arthritis is discussed, as well as how these factors can influence a patient's response to synthetic and biologic immunosuppressive therapy.
在高等脊椎动物中,位于内外部环境交界处的黏膜部位直接与细菌、病毒和真菌相互作用。通过共同进化,宿主针对某些感染因子形成了耐受或忽视机制,因为宿主与共生细菌建立了“功能获得性”相互作用。事实上,一些细菌协助宿主发挥不同功能,其中包括复杂碳水化合物的消化以及维生素的吸收与供应。毫无疑问,微生物群从出生起就调节先天性和获得性免疫反应。然而,细菌种类在质量和数量上的变化会干扰炎症与耐受之间的平衡。实际上,肠道细菌组成与炎症严重程度之间的相关性最早是在炎症性肠病中被描述的,后来扩展到了其他病症。遗传背景、环境因素(如压力或吸烟)以及饮食会导致常驻细菌发生强烈变化,这可能使肠上皮暴露于多种不同的代谢产物中,其中许多代谢产物的功能和后果尚不清楚。此外,肠道通透性的改变可能使病原体进入,从而引发感染和/或慢性炎症。在这种情况下,黏膜部位发生的局部事件可能是自身免疫反应的触发原因,最终累及远处的部位或器官。最近,多项研究将类风湿关节炎(RA)中口腔微生物群的改变以及脊柱关节炎(SpA)中肠道菌群失调归因于致病作用。也有越来越多的证据表明,不同药物,如抗生素和免疫抑制剂,会影响RA和SpA患者微生物群的多样性和组成,同时也会受到其影响。因此,在诸如RA和SpA等复杂疾病中,不仅个体的遗传背景、性别和免疫背景相关,感染史以及黏膜部位微生物群落的结构也应予以考虑。在此讨论微生物群和感染在慢性关节炎的发生和发展中的作用,以及这些因素如何影响患者对合成和生物免疫抑制疗法的反应。