Sophy β-Glucan from the Black Yeast Aureobasidium pullulans Attenuates Salmonella-Induced Intestinal Epithelial Barrier Injury in Caco-2 Cell Monolayers via Exerting Anti-Oxidant and Anti-Inflammatory Properties

Author:

Guo Fangshen1,Liu Hongbin1,Li Xiaomin1,Hu Zeqiong1,Huang Jia1,Bi Ruichen1,Abbas Waseem1,Guo Yuming1,Wang Zhong1

Affiliation:

1. State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China

Abstract

The zoonotic pathogens Salmonella spp. infection disrupted intestinal epithelial barrier function and induced local gastroenteritis and systemic inflammation in humans and animals. Sophy β-glucan, a water-soluble β-1,3/1,6-glucan synthesized from the black yeast Aureobasidium pullulans, was reported with immune-regulatory, anti-inflammatory, and anti-infective properties. Here, we investigated the protective role of sophy β-glucan on Salmonella enterica serotype Enteritidis (SE)-challenged Caco-2 cells monolayer and explored underlying action mechanisms. The results showed that pretreatment with sophy β-glucan blocked the adhesion and invasion of SE onto Caco-2 cells along with alleviating SE-induced epithelial barrier injury, as evidenced by increased trans-epithelial electrical resistance, decreased fluorescently-labeled dextran 4 flux permeability, and an enhanced Claudin-4 protein level in the SE-stimulated Caco-2 cell monolayer. Moreover, treatment with β-glucan down-regulated pro-inflammatory factors (IL-1β, IL-8, and TNF-α) while up-regulating anti-inflammatory factors IL-10 at mRNA and protein levels in SE-infected Caco-2 cells. Furthermore, sophy β-glucan strengthened the anti-oxidative capacity of Caco-2 monolayers cells by elevating T-AOC and SOD activity and inhibiting MDA production defending SE. Together, our data showed that sophy β-glucan could prevent intestinal epithelial injury induced by SE, possibly by exerting anti-oxidant and anti-inflammatory properties, and it might be helpful for controlling SE infection.

Funder

National Natural Science Foundation of China

Publisher

MDPI AG

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Biochemistry,Physiology

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