Effects of Lactobacillus johnsonii and Lactobacillus reuteri on gut barrier function and heat shock proteins in intestinal porcine epithelial cells. Issue 4 (6th April 2015)

• Record Type: Journal Article
• Authors: Liu, Hao‐Yu; Roos, Stefan; Jonsson, Hans; Ahl, David; Dicksved, Johan; Lindberg, Jan Erik; Lundh, Torbjörn
• Is Part Of: Physiological reports. Volume 3:Issue 4(2015:Apr.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2015-04-06
• Subjects: Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.12355
• Languages: English
• ISSNs: 2051-817X

Abstract

<abstract abstract-type="main" id="phy212355-abs-0001"> <title>Abstract</title> <p>Heat shock proteins (HSPs) are a set of highly conserved proteins that can serve as intestinal gate keepers in gut homeostasis. Here, effects of a probiotic, <italic>Lactobacillus rhamnosus </italic>GG (LGG), and two novel porcine isolates, <italic>Lactobacillus johnsonii</italic> strain P47‐HY and <italic>Lactobacillus reuteri</italic> strain P43‐HUV, on cytoprotective HSP expression and gut barrier function, were investigated in a porcine IPEC‐J2 intestinal epithelial cell line model. The IPEC‐J2 cells polarized on a permeable filter exhibited villus‐like cell phenotype with development of apical microvilli. Western blot analysis detected HSP expression in IPEC‐J2 and revealed that <italic>L. johnsonii</italic> and <italic>L. reuteri</italic> strains were able to significantly induce HSP27, despite high basal expression in IPEC‐J2, whereas LGG did not. For HSP72, only the supernatant of <italic>L. reuteri</italic> induced the expression, which was comparable to the heat shock treatment, which indicated that HSP72 expression was more stimulus specific. The protective effect of lactobacilli was further studied in IPEC‐J2 under an enterotoxigenic <italic>Escherichia coli</italic> (ETEC) challenge. ETEC caused intestinal barrier destruction, as reflected by loss of cell–cell contact, reduced IPEC‐J2 cell viability and transepithelial electrical resistance, and disruption of tight junction protein zonula occludens‐1. In contrast, the <italic>L. reuteri</italic> treatment substantially counteracted these detrimental effects and preserved the barrier function. <italic>L. johnsonii</italic> and LGG also achieved barrier protection, partly by directly inhibiting ETEC attachment. Together, the results indicate that specific strains of <italic>Lactobacillus</italic> can enhance gut barrier function through cytoprotective HSP induction and fortify the cell protection against ETEC challenge through tight junction protein modulation and direct interaction with pathogens.</p> </abstract>