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口服 OLL2712 可降低肠道通透性,尤其是回肠:摄入的乳酸菌通过与肠道菌群合作减轻肥胖引起的炎症。

Orally administered OLL2712 decreased intestinal permeability, especially in the ileum: Ingested lactic acid bacteria alleviated obesity-induced inflammation by collaborating with gut microbiota.

机构信息

Research Center for Food Safety, The University of Tokyo, Tokyo, Japan.

Department of Applied Biological Chemistry, The University of Tokyo, Tokyo, Japan.

出版信息

Front Immunol. 2023 Feb 23;14:1123052. doi: 10.3389/fimmu.2023.1123052. eCollection 2023.

Abstract

INTRODUCTION

Chronic inflammation caused by dietary obesity has been considered to induce lifestyle-related diseases and functional ingredients with anti-inflammatory effects are attracting attention. Although multiple studies on obesity had proved the anti-inflammatory effects of ingestion of lactic acid bacteria (LAB) and other functional ingredients on adipose tissue, the precise effects on the intestine, especially on the individual intestinal segments have not been made clear. In this study, we elucidated the mechanisms of (basonym: ) OLL2712 in suppressing obesity-induced inflammation using high fat diet (HFD)-fed mice obesity model.

METHODS

We orally administered heat-treated LAB to HFD-fed mice model, and investigated the inflammatory changes in adipose tissue and intestinal immune cells. We also analyzed gut microbiota, and evaluated the inflammation and permeability of the duodenum, jejunum, ileum and colon; four intestinal segments differing in gut bacteria composition and immune response.

RESULTS

After 3-week LAB administration, the gene expression levels of proinflammatory cytokines were downregulated in adipose tissue, colon, and Peyer's patches (PP)-derived F4/80 cells. The LAB treatment alleviated obesity-related gut microbiota imbalance. OLL2712 treatment helps maintain intestinal barrier function, especially in the ileum, possibly by preventing ZO-1 and Occludin downregulation.

DISCUSSION

Our results suggest that the oral administration of the LAB strain regulated the gut microbiota, suppressed intestinal inflammation, and improved the gut barrier, which could inhibit the products of obesity-induced gut dysbiosis from translocating into the bloodstream and the adipose tissue, through which the LAB finally alleviated the inflammation caused by dietary obesity. Barrier improvement was observed, especially in the ileum, suggesting collaborative modulation of the intestinal immune responses by ingested LAB and microbiota.

摘要

简介

饮食肥胖引起的慢性炎症被认为会导致与生活方式相关的疾病,具有抗炎作用的功能性成分引起了人们的关注。虽然多项关于肥胖的研究已经证明了摄入乳酸菌(LAB)和其他功能性成分对脂肪组织的抗炎作用,但它们对肠道的具体作用,特别是对各个肠道段的作用还不清楚。在这项研究中,我们使用高脂肪饮食(HFD)喂养肥胖模型小鼠,阐明了 (同义名:)OLL2712 抑制肥胖引起的炎症的机制。

方法

我们给 HFD 喂养的肥胖模型小鼠口服加热处理的 LAB,并研究了脂肪组织和肠道免疫细胞的炎症变化。我们还分析了肠道微生物群,并评估了十二指肠、空肠、回肠和结肠的炎症和通透性;这四个肠道段的肠道细菌组成和免疫反应不同。

结果

在 LAB 给药 3 周后,脂肪组织、结肠和派尔集合淋巴结(PP)衍生的 F4/80 细胞中促炎细胞因子的基因表达水平下调。LAB 处理缓解了肥胖相关的肠道微生物群失衡。OLL2712 处理有助于维持肠道屏障功能,特别是在回肠中,可能是通过防止 ZO-1 和 Occludin 的下调。

讨论

我们的结果表明,LAB 菌株的口服给药调节了肠道微生物群,抑制了肠道炎症,改善了肠道屏障功能,从而阻止了肥胖引起的肠道菌群失调产物向血液和脂肪组织转移,LAB 最终缓解了饮食引起的肥胖炎症。在回肠中观察到屏障改善,这表明摄入的 LAB 和微生物群协同调节肠道免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1604/9995389/70f31701e9c6/fimmu-14-1123052-g001.jpg

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