进食可引起炎症，但未必是坏事，前提是……
人体进食时，不仅摄入营养素，也摄入大量细菌，面临着同时分配被摄入葡萄糖和对抗这些细菌所带来的挑战。由于进食激活了健康个体的免疫系统，从而引发炎症反应，并同时起到保护作用。然而，在超重个体中，这种炎症反应会面临很大失败，可能导致糖尿病。众所周知，发生于成人的2型糖尿病可导致一系列有负面影响的慢性炎症。因此，很多治疗糖尿病的临床研究对阻断涉及炎症过程的白细胞介素（IL）-1β进行探索。在糖尿病患者中，这种信使物质可触发慢性炎症，并引起产生胰岛素的β细胞死亡。然而，这种炎症也有一些积极方面。
2017年1月16日，英国《自然·免疫学分册》在线发表瑞士（巴塞尔大学、苏黎世大学、洛桑大学、日内瓦大学）和法国（里尔大学、欧洲糖尿病基因组研究所）的研究报告，发现短期炎症反应对健康个体糖摄取和免疫系统活化发挥重要作用。
该研究证实，在进餐期间，肠周围巨噬细胞数量增加，并根据血液中的葡萄糖浓度产生不同量的信使物质IL-1β，这会反过来刺激胰腺β细胞产生胰岛素。然后，胰岛素会引起巨噬细胞产生IL-1β增加。胰岛素和IL-1β协同作用以调节血糖水平，信使物质IL-1β能保证免疫系统提供葡萄糖从而保持活性。
该代谢免疫系统机制取决于进餐时细菌和营养物质摄入，在营养物质充足的条件下，免疫系统能够充分地抵抗外来细菌。相反，当营养物质缺乏时，剩余热量必须以免疫反应为代价，保证重要的生命功能，这能解释饥荒时感染疾病的高发生率。
Nat Immunol. 2017 Jan 16. [Epub ahead of print]
Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation.
Dror E, Dalmas E, Meier DT, Wueest S, Thévenet J, Thienel C, Timper K, Nordmann TM, Traub S, Schulze F, Item F, Vallois D, Pattou F, Kerr-Conte J, Lavallard V, Berney T, Thorens B, Konrad D, Boni-Schnetzler M, Donath MY.
University Hospital Basel, Basel, Switzerland; University of Basel, Basel, Switzerland; University Children's Hospital, Zurich, Switzerland; Centre Hospitalier Universitaire, Lille, France; European Genomic Institute for Diabetes, Lille, France; University of Lausanne, Lausanne, Switzerland; Geneva University Hospitals, Geneva, Switzerland; University of Geneva School of Medicine, Geneva, Switzerland.
The deleterious effect of chronic activation of the IL-1β system on type 2 diabetes and other metabolic diseases is well documented. However, a possible physiological role for IL-1β in glucose metabolism has remained unexplored. Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1β, in a glucose-dependent manner. Subsequently, IL-1β contributed to the postprandial stimulation of insulin secretion. Accordingly, lack of endogenous IL-1β signaling in mice during refeeding and obesity diminished the concentration of insulin in plasma. IL-1β and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1β mediated by the NLRP3 inflammasome. Postprandial inflammation might be limited by normalization of glycemia, since it was prevented by inhibition of the sodium-glucose cotransporter SGLT2. Our findings identify a physiological role for IL-1β and insulin in the regulation of both metabolism and immunity.
PMID: 28092375
DOI: 10.1038/ni.3659
