Ribaldone Davide Giuseppe, Pellicano Rinaldo, Actis Giovanni Clemente
Department of Surgical Sciences, University of Turin, Turin, Italy.
Unit of Gastroenterology, Molinette-San Giovanni Antica Sede (SGAS) Hospital, Turin, Italy.
Clin Exp Gastroenterol. 2019 Jul 19;12:321-329. doi: 10.2147/CEG.S210844. eCollection 2019.
Western populations harbor a chronic inflammation pattern that lacks organ cardinal signs (edema, increased temperature, pain, and impaired function), releases increased levels of C-reactive protein, and often runs a creeping clinical course with generalized debilitating disease superimposed on system-specific involvement, mostly including nervous tissue (multiple sclerosis, Parkinson's syndromes), joints (arthritis), and skin (psoriasis). A finalistic interpretation may apply to the consideration of the gut as the source of inflammation. In fact, these kind of local events as well as the remote manifestations named above, could be conditioned by the microbiome, the huge cell population indwelling the gut which is under growing scrutiny. The role of the gut as a barrier organ justifies lingering submucosal inflammation as a patrolling activity to maintain bodily integrity; the microbiome, launching inflammogenic signals in response to abrupt diet changes, confers to gut inflammation a socioeconomic vector calling for hitherto unrecognized multi-disciplinary interventions.
西方人群呈现出一种慢性炎症模式，其缺乏器官的主要体征（水肿、体温升高、疼痛和功能受损），C反应蛋白水平升高，且往往呈现渐进性临床病程，全身性衰弱疾病叠加在特定系统受累之上，主要包括神经组织（多发性硬化症、帕金森综合征）、关节（关节炎）和皮肤（银屑病）。一种目的论解释可能适用于将肠道视为炎症来源的考量。事实上，这类局部事件以及上述的远处表现，可能受到微生物群的影响，微生物群是存在于肠道内且受到越来越多审视的庞大细胞群体。肠道作为屏障器官的作用证明了黏膜下持续存在的炎症是一种维持身体完整性的巡逻活动；微生物群在应对突然的饮食变化时发出促炎信号，赋予肠道炎症一种社会经济因素，需要迄今尚未被认识到的多学科干预措施。
