Many studies have highlighted the role of probiotics in re-establishing the gut microbiota balance and preventing
intestinal barrier dysfunction. In fact, they can also contribute to the upregulation of antiinflammatory
genes and the downregulation of pro-inflammatory genes, which are known to contribute to
the development of the inflammatory bowel disease (IBD) syndrome. The present study aims to investigate
the effect of the compatible solute hydroxyectoine (HOE), to be used as a cryopreservant but also for its
intrinsic biological properties, to obtain a new formula containing three probiotic strains (Limosilactobacillus
fermentum (L. fermentum), Levilactobacillus brevis SP-48 (L. brevis), and Bifidobacterium lactis HN019 (B.
lactis)), and evaluate the latter for its ability to prevent lipopolysaccharide (LPS)-induced inflammation in an
in vitro bi-dimensional model of the intestinal barrier using a Caco-2 cell monolayer. The mRNA expression
levels of the inflammatory cytokines (IL-6, IL-1β, and TNF-α) were analyzed by real-time PCR. Changes in the
modulation of (TLR-4 and NF-κB) proteins were assessed by western blotting, and the effect of the HOE/
PRO formula on the intestinal epithelial barrier function was also assessed using an immunofluorescence
microscope for the tight junction protein zonula occludens-1 (ZO-1). This study found that this novel probiotic
formulation containing HOE is capable of decreasing LPS-induced cytokines, as confirmed by the results
of RT-PCR and ELISA and preserving the integrity of tight junctions as demonstrated by the relevant
expression of ZO-1. HOE/PRO was shown to be effective in reducing the expression of TLR-4 and NF-κB.
The latter plays a key role as an inflammation modulator as shown through experiments run with the THP-1/
NF-κB reporter gene. Collectively, our data indicate that the HOE/PRO formula is a good candidate for
potential preventive and/or therapeutic implementation in IBD.

Title

Food and function

Publisher

Royal society of chemistry

Publisher Country

United Kingdom

Publication Type

Prtinted only

Volume

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Year

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Pages

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