Low-fat yogurt alleviates the pro-inflammatory cytokine IL-1β-induced intestinal epithelial barrier dysfunction

Abstract

Yogurt is a source of bioactive compounds and probiotic microorganisms that modify immunity and metabolism to benefit human health beyond nutrition. In this study, we examined the capacity of yogurt to prevent epithelial barrier disruption in vitro. Different preparations of yogurt were added apically to Caco-2 monolayers before IL-1β exposure. Dulbecco's modified Eagle medium containing 25% (vol/vol) low-fat yogurt prevented cytokine-induced transepithelial resistance reduction and increases to paracellular permeability measured with fluorescein isothiocyanate-dextran (4 kDa), whereas nonfat yogurt was unable to decrease paracellular permeability to fluorescein isothiocyanatedextran. Moreover, the concentration of IL-8 in low-fatyogurt-treated inflamed cells was decreased to 252.40 ± 27.24 pg/mL, which was lower than that of untreated, inflamed cells (407.20 ± 50.05 pg/mL), further indicating the anti-inflammatory roles of low-fat yogurt. The low-fat yogurt was able to downregulate the transcription of myosin light-chain kinase (MLCK) gene, but upregulate the expression of tight junction protein ZO-1 (TJP1). These findings indicate that low-fat yogurt can maintain intestinal barrier integrity better than nonfat yogurt after pro-inflammatory cytokine exposure.

Probiotics, prebiotics, and synbiotics regulate the intestinal microbiota differentially and restore the relative abundance of specific gut microorganisms

“…Some researchers reported that the administration of a combination of L. rhamnosus and L. helveticus probiotics did not prevent the development of moderate to severe gastroenteritis (Freedman et al, 2018). However, the findings of Zhai et al (2019) strongly suggest that low-fat yogurt fermented by Streptococcus thermophilus and L. bulgaricus can maintain intestinal barrier integrity. At present, it is unclear which probiotics affect the gut microbes, which makes it difficult to choose which probiotics to use to treat enteritis.…”

Sinapic Acid Alleviated Inflammation-Induced Intestinal Epithelial Barrier Dysfunction in Lipopolysaccharide- (LPS-) Treated Caco-2 Cells

“…It has been reported that overexpression of MLCK leads to increase intestinal epithelial TJ permeability [15,44]. Many studies have reported that increased MLCK activity phosphorylates MLC and subsequently leads to the centripetal contraction of the TJ complex, eventually result in the opening of the intestinal epithelial barrier [45][46][47]. The results from our study clearly indicate that LPS promoted the expression of MLCK and MLC and diminished the expression of key sealing TJ proteins, such as ZO-1, occludin, and claudin-1, causing varying degrees of displacement of the claudin-1 and ZO-1 proteins.…”

IL-1β and the Intestinal Epithelial Tight Junction Barrier

“…In these studies, targeted knockdown of MEKK-1, IKKβ, or NF-κB p65 prevented the IL-1β-induced increase in MLCK gene activity and increase in intestinal epithelial TJ permeability, confirming the regulatory role of MEKK-1, IKKβ and the NF-κB p50/p65 axis on MLCK gene activation ( 88 ). Zhai and colleagues recently showed that low-fat yogurt prevented the IL-1β-induced intestinal barrier disruption by inhibiting the upregulation of MLCK gene expression in Caco-2 cells ( 122 ). These studies also showed that the IL-1β-induced increase in NF-κB activation is inhibited by low-fat yogurt application to Caco-2 cells ( 122 ).…”

“…Zhai and colleagues recently showed that low-fat yogurt prevented the IL-1β-induced intestinal barrier disruption by inhibiting the upregulation of MLCK gene expression in Caco-2 cells ( 122 ). These studies also showed that the IL-1β-induced increase in NF-κB activation is inhibited by low-fat yogurt application to Caco-2 cells ( 122 ). Collectively, these studies show that IL-1β-induced increases in MLCK gene activity and protein synthesis are required for increased intestinal TJ permeability.…”