Four types of Bifidobacteria trigger autophagy response in intestinal epithelial cells. Issue 11 (November 2014)

• Record Type: Journal Article
• Authors: Lin, Rong; Jiang, Ye; Zhao, Xin Yan; Guan, Yang; Qian, Wei; Fu, Xiao Chao; Ren, Hun Yu; Hou, Xiao Hua
• Is Part Of: Journal of digestive diseases. Volume 15:Issue 11(2014:Nov.)
• Page Start: 597
• Page End: 605
• Publication Date: 2014-11
• Subjects: Digestive organs -- Diseases -- Periodicals; Gastroenterology -- Periodicals; 616.3
• DOI: 10.1111/1751-2980.12179
• Languages: English
• ISSNs: 1751-2972

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="cdd12179-sec-0001" sec-type="section"> <title>Objectives</title> <p>To investigate the influence of gut microbiota on autophagy activation in intestinal epithelial cells (IEC) and to evaluate the IEC autophagy response to different types of <italic>Bifidobacteria</italic>.</p> </sec> <sec id="cdd12179-sec-0002" sec-type="section"> <title>Methods</title> <p>IEC‐18 cells were treated with lipopolysaccharide (LPS) derived from enteropathogenic <italic>Escherichia coli</italic> (EPEC) O127:B8 and culture medium supernatants of four types of <italic>Bifidobacteria</italic>. Transepithelial electrical resistance (TEER) was measured using an epithelial voltohmmeter. Autophagy was determined by transmission electron microscopy (TEM), the ratio of LC3‐II to LC3‐I and the persistence of both green fluorescent protein (GFP) and mCherry signals using a tandem mCherry‐GFP‐LC3 construct. The expression of <italic>Atg12–Atg5–Atg16</italic> complex was measured by quantitative real‐time polymerase chain reaction.</p> </sec> <sec id="cdd12179-sec-0003" sec-type="section"> <title>Results</title> <p>EPEC‐LPS significantly diminished the TEER of IEC compared with untreated controls by 45–55%. This reduction was not observed after treated with <italic>Bifidobacteria</italic> at all time points. <italic>Bifidobacteria</italic> could initiate the activation of autophagy in IEC, based on both the ratio of LC3‐II to LC3‐I and TEM. There was no difference in the influence of the four types of <italic>Bifidobacteria</italic> on the autophagy response. Compared with <italic>Bifidobacteria</italic>, IEC reacted to EPEC‐LPS much more intensively by autophagy accumulation. More mCherry<sup>+</sup>LC3 autophagic puncta and increased expressions of autophagy genes <italic>Atg5</italic>, <italic>Atg12</italic> and <italic>Atg16</italic> could be detected after being treated with <italic>Bifidobacteria</italic> and EPEC‐LPS.</p> </sec> <sec id="cdd12179-sec-0004" sec-type="section"> <title>Conclusions</title> <p> <italic>Bifidobacteria</italic> initiate autophagy activation in IEC. The <italic>Atg12–Atg5–Atg16</italic> multimeric complex might participate in the activation of <italic>Bifidobacteria</italic>‐induced cell autophagy.</p> </sec> </abstract>