INFLAMMATION DURING OBESITY: IMMUNE RESPONSES TO GUT ANTIGENS IN MESENTERIC FAT

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 项目5：肥胖期间的炎症：对肠系膜脂肪中肠道抗原的免疫反应 埃里克·埃克哈特 肥胖者的脂肪组织大大增大，他们也更容易患上心血管疾病、糖尿病和其他疾病。有趣的是，所有这些疾病都带有炎症成分，因此长期以来一直怀疑脂肪组织可能对全身炎症产生影响。事实上，最近的研究已经清楚地表明，肥胖个体的脂肪组织经常发炎，并释放物质进入循环，可能导致其他地方的炎症。那么，是什么导致肥胖者的脂肪组织发炎呢？答案可能在于肠道，因为它主要是肠道附近的脂肪组织，如肠系膜脂肪，肥胖时会发炎，而皮下脂肪，虽然同样扩大，但通常不会发炎。我们假设，当肥胖者摄入高脂肪食物时，肠道中的细菌或细菌产物进入肠系膜脂肪组织，因为大量的膳食脂肪会诱导肠道泄漏。到目前为止，我们的小鼠数据表明情况确实如此。如果我们证实了这些数据和我们的假设，那么我们就可以研究如何减少肠道中导致脂肪组织炎症的促炎细菌的数量。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Project 5: Inflammation During Obesity: Immune Responses to Gut Antigens in Mesenteric Fat Erik Eckhardt Obese individuals have greatly enlarged fat tissue, and they are also more likely to suffer from cardiovascular disease, diabetes, and other diseases. Interestingly, all these diseases carry an inflammatory component, and it has therefore long be suspected that fat tissues may have an effect on whole body inflammation. Indeed, recent work has clearly shown that fat tissues from obese individuals are often inflamed and release substances into the circulation that can cause inflammation elsewhere. What, then, causes fat tissues from obese individuals to be inflamed? The answer may lie in the intestine, because it is mostly fat tissue near the intestine, such as mesenteric fat, which is inflamed in obesity, whereas subcutaneous fat, while equally enlarged, often is not inflamed. We hypothesize that bacteria or bacterial products in the intestine enter mesenteric fat tissue when obese individuals ingest high fat meals, because large amounts of dietary fat can induce leakiness in the intestine. Our data with mice so far suggest that this is indeed the case. If we confirm these data and our hypothesis in general, we can then look at how to reduce the number of pro-inflammatory bacteria in the intestine that cause fat tissue inflammation.