USDA-ARS, Southern Plains Agricultural Research Center, College Station, TX.
Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Poult Sci. 2018 Jul 1;97(7):2339-2346. doi: 10.3382/ps/pey087.
The intestinal tract harbors a diverse community of microbes that have co-evolved with the host immune system. Although many of these microbes execute functions that are critical for host physiology, the host immune system must control the microbial community so that the dynamics of this interdependent relationship is maintained. To facilitate host homeostasis, the immune system ensures that the microbial load is tolerated, but anatomically contained, while remaining reactive to microbial invasion. Inflammation is the most prevalent manifestation of host defense in reaction to alterations in tissue homeostasis and is elicited by innate immune receptors that recognize and detect infection, host damage, and danger signaling molecules that activate a highly regulated network of immunological and physiological events for the purpose of maintaining homeostasis and restoring functionality. The efficacy, duration, and consequences of an inflammatory response is dependent upon the type of trigger that is recognized by the innate immune receptors. Further, because of different triggers, there are multiple phenotypes of inflammation. Physiological inflammation is the homeostatic balance between tolerance of the microbiota and the reactivity to pathogen invasion. Pathologic inflammation is usually an acute response that involves the host response to toxins and infection often resulting in collateral damage to surrounding tissue and increased metabolic energy use. Metabolic inflammation is a chronic low-grade inflammation generated by excessive nutrient intake and the metabolic surplus fosters metabolic dysfunction by integrating signals from both the immune and metabolic systems. Sterile inflammation is a low-grade chronic inflammation, in the absence of an infection, in response to chemical, physical, and metabolic stimuli. With a sterile inflammatory response, the stimulus persists without being eliminated suggesting that collateral damage is the cause of the disease. The common denominator with all intestinal inflammatory phenotypes is the central role of the gut microbiota whether it be microbial balance and diversity of microbial metabolic production or microbial turnover.
肠道中栖息着多种多样的微生物群落，这些微生物与宿主的免疫系统共同进化。尽管许多微生物执行着对宿主生理功能至关重要的功能，但宿主免疫系统必须控制微生物群落，以维持这种相互依存关系的动态平衡。为了促进宿主的体内平衡，免疫系统确保微生物负荷被耐受，但在解剖上被限制，同时对微生物入侵保持反应性。炎症是宿主防御反应中最常见的表现形式，是由先天免疫受体识别和检测感染、宿主损伤以及激活高度调节的免疫和生理事件网络以维持体内平衡和恢复功能的危险信号分子引起的。炎症反应的效果、持续时间和后果取决于先天免疫受体识别的触发类型。此外，由于不同的触发因素，存在多种炎症表型。生理性炎症是微生物群耐受和对病原体入侵反应之间的体内平衡。病理性炎症通常是一种急性反应，涉及宿主对毒素和感染的反应，通常导致周围组织的附带损伤和代谢能量使用的增加。代谢性炎症是由过量营养摄入和代谢过剩引起的慢性低度炎症，通过整合来自免疫和代谢系统的信号来促进代谢功能障碍。无菌性炎症是一种低度慢性炎症，在没有感染的情况下，对化学、物理和代谢刺激作出反应。在无菌性炎症反应中，刺激持续存在而未被消除，这表明附带损伤是疾病的原因。所有肠道炎症表型的共同点是肠道微生物群的核心作用，无论是微生物的平衡和微生物代谢产物的多样性，还是微生物的更替。
