Dietary fibre-based SCFA mixtures promote both protection and repair of intestinal epithelial barrier function in a Caco-2 cell model

Chen, Tingting; Kim, Choon Young; Kaur, Amandeep; Lamothe, Lisa; Shaikh, Maliha; Keshavarzian, Ali; Hamaker, Bruce R.

doi:10.1039/c6fo01532h

Cited by 110 publications

(96 citation statements)

References 55 publications

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“…Previous studies have shown that L. salivarius produces abundant propionate/butyrate (16,17). Additionally, in previous studies, improved barrier function by SCFA was reported (18)(19)(20). SCFAs such as butyrate and acetate are known to protect intestinal barrier integrity by regulating through the activation of AMPK and TLR4.…”

Section: Lactobacillus Salivarius Bp121 Prevents Cisplatin-induced Acmentioning

confidence: 90%

Lactobacillus salivarius BP121 prevents cisplatin‑induced acute kidney injury by inhibition of uremic toxins such as indoxyl sulfate and p‑cresol sulfate via alleviating dysbiosis

Lee¹,

Park

Kim³

et al. 2020

Int J Mol Med

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The gut microbiota is important for maintaining the integrity of the intestinal barrier, promoting immunological tolerance and carrying out metabolic activities that have not evolved in hosts. Intestinal dysbiosis is associated with chronic kidney disease and probiotic supplementation has been shown to be beneficial. However, it is not known whether gut microorganisms-specifically, lactic acid bacteria (LAB) can protect against acute kidney injury (AKI). To address this issue, the present study investigated the effects of Lactobacillus salivarius BP121, an intestinal LAB isolated from the feces of newborns, in a rat model of cisplatin-induced AKI and also in Caco-2 human intestinal epithelial cells. BP121 prevented cisplatin-induced AKI in rats, as demonstrated by decreases in inflammation and oxidative stress in kidney tissue and in serum levels of uremic toxins such as indoxyl sulfate (IS) and p-cresol sulfate (PCS). BP121 also reduced intestinal permeability, as determined using fluorescein isothiocyanate-dextran by immunohistochemical detection of tight junction (TJ) proteins such as zona occludens-1 and occludin. The abundance of Lactobacillus spp., which are beneficial intestinal flora, was increased by BP121; this was accompanied by an increase in the concentrations of short-chain fatty acids in feces. Additionally, H 2 O 2 -induced TJ protein damage was reduced in Caco-2 cells treated with BP121 culture supernatant, an effect that was reversed by the 5' AMP-activated protein kinase (AMPK) inhibitor Compound C and Toll-like receptor (TLR)4 inhibitor TLR4-IN-C34. In conclusion, this study demonstrated that L. salivarius BP121 protects against cisplatin-induced AKI by decreasing inflammation and oxidative stress and this renoprotective effect is partially mediated by modulating the gut environment and thereby suppressing IS and PCS production as well as by regulating AMPK and TLR4 dependent TJ assembly.

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Section: Lactobacillus Salivarius Bp121 Prevents Cisplatin-induced Acmentioning

confidence: 90%

Lactobacillus salivarius BP121 prevents cisplatin‑induced acute kidney injury by inhibition of uremic toxins such as indoxyl sulfate and p‑cresol sulfate via alleviating dysbiosis

Lee¹,

Park

Kim³

et al. 2020

Int J Mol Med

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“…Likewise, the protein expression of ZO‐1, occludin, and claudin‐1 was significantly reduced in IPEC‐J2 cells exposed to heat for 72 hr. Because the single‐cell layer of the intestinal epithelium constitutes the largest and most important barrier (T. Chen et al, 2017), heat exposure‐induced intestinal barrier damage is attributable, at least in part, to the inhibition of cell proliferation and the induction of cell apoptosis. Nevertheless, it is worth noting that the intestinal barrier dysfunction is not specific to heat‐exposure damage.…”

Section: Discussionmentioning

confidence: 99%

Wnt/β‐catenin‐mediated heat exposure inhibits intestinal epithelial cell proliferation and stem cell expansion through endoplasmic reticulum stress

Zhou

Huang

Zhu

et al. 2020

Journal Cellular Physiology

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Heat stress induced by continuous high ambient temperatures or strenuous exercise in humans and animals leads to intestinal epithelial damage through the induction of intracellular stress response. However, the precise mechanisms involved in the regulation of intestinal epithelial cell injury, especially intestinal stem cells (ISCs), remain unclear. Thereby, in vitro a confluent monolayer of IPEC‐J2 cells was exposed to the high temperatures (39, 40, and 41°C), the IPEC‐J2 cell proliferation, apoptosis, differentiation, and barrier were determined, as well as the expression of GRP78, which is a marker protein of endoplasmic reticulum stress (ERS). The Wnt/β‐catenin pathway‐mediated regenerative response was validated using R‐spondin 1 (Rspo1). And ex‐vivo, three‐dimensional cultured enteroids were developed from piglet jejunal crypt and employed to assess the ISC activity under heat exposure. The results showed that exposure to 41°C for 72 hr, rather than 39°C and 40°C, decreased IPEC‐J2 cell viability, inhibited cell proliferation and differentiation, induced ERS and cell apoptosis, damaged barrier function and restricted the Wnt/β‐catenin pathway. Nevertheless, Wnt/β‐catenin reactivation via Rspo1 protects the intestinal epithelium from heat exposure‐induced injury. Furthermore, exposure to 41°C for 24 hr reduced ISC activity, stimulated crypt‐cell apoptosis, upregulated the expression of GRP78 and caspase‐3, and downregulated the expression of β‐catenin, Lgr5, Bmi1, Ki67, KRT20, ZO‐1, occludin, and claudin‐1. Taken together, we conclude that heat exposure induces ERS and downregulates the Wnt/β‐catenin signaling pathway to disrupt epithelial integrity by inhibiting the intestinal epithelial cell proliferation and stem cell expansion.

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“…24 FITC-D4 was added to the apical chamber at the end of treatment. The insert area was 0.33 cm 2 and the pore size was 0.4 µm.…”

Section: Determination Of Teer and Fitc-d4mentioning

confidence: 99%

“…Fluorescein isothiocyanate-dextran (FITC-D4, 4 kDa, 0.25 mM) measurements were taken for paracellular permeability. 24 FITC-D4 was added to the apical chamber at the end of treatment. After 2 hours, 50-µL medium from the bottom chamber were transferred to a fluorescence measurement plate, and fluorescence intensity was measured at an excitation wavelength of 485 nm and emission wavelength of 530 nm.…”

Section: Determination Of Teer and Fitc-d4mentioning

confidence: 99%

Icariin and its phosphorylated derivatives alleviate intestinal epithelial barrier disruption caused by enterotoxigenic Escherichia coli through modulate p38 MAPK in vivo and in vitro

Xiong

Huang

et al. 2019

FASEB j.

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractThe natural product icariin (ICA) and its phosphorylated derivatives (pICA) have been shown to have outstanding anti-inflammatory and antioxidant properties. This study was to explore the protective effects of ICA and pICA on the intestinal epithelium of enterotoxigenic Escherichia coli (ETEC)-induced piglet diarrhea and its underlying mechanisms in vivo and in vitro. ETEC K88 increased pro-inflammatory cytokine expression, activated oxidative stress and inhibited antioxidant enzyme activity, induced phosphorylated p38 MAPK gene and protein expression, disrupted intestinal barrier function, and led to diarrhea in piglets. Pretreatment with ICA and pICA effectively alleviated ETEC-induced intestinal barrier dysfunction in vivo and in vitro. Pretreatment with p38 MAPK inhibitor (SB203580) significantly rescued the IPEC-J2 cells barrier function damaged by ETEC challenge. However, pretreatment with p38 MAPK activator (anisomycin) did not alleviated the IPEC-J2 cells barrier function damaged by ETEC challenge. Our data demonstrated that ICA and pICA regulate the inflammatory response and oxidative stress of intestinal epithelial cells by inhibiting the expression of p38 MAPK, thereby alleviating ETEC K88-induced disruption of intestinal barrier function and intestinal permeability. These findings provide new insights into the prevention and treatment of intestinal barrier dysfunction induced by ETEC K88. K E Y W O R D S enterotoxigenic Escherichia coli K88, icariin, intestinal barrier function, p38 MAPK, phosphorylated icariin 1784 | XIONG et al.

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Dietary fibre-based SCFA mixtures promote both protection and repair of intestinal epithelial barrier function in a Caco-2 cell model

Cited by 110 publications

References 55 publications

Lactobacillus salivarius BP121 prevents cisplatin‑induced acute kidney injury by inhibition of uremic toxins such as indoxyl sulfate and p‑cresol sulfate via alleviating dysbiosis

Lactobacillus salivarius BP121 prevents cisplatin‑induced acute kidney injury by inhibition of uremic toxins such as indoxyl sulfate and p‑cresol sulfate via alleviating dysbiosis

Wnt/β‐catenin‐mediated heat exposure inhibits intestinal epithelial cell proliferation and stem cell expansion through endoplasmic reticulum stress

Icariin and its phosphorylated derivatives alleviate intestinal epithelial barrier disruption caused by enterotoxigenic Escherichia coli through modulate p38 MAPK in vivo and in vitro

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