Anneslea fragrans Wall. ameliorates ulcerative colitis via inhibiting NF-κB and MAPK activation and mediating intestinal barrier integrity

Deng, Xiaocui; Wang, Yudan; Tian, Lei; Yang, Meilian; He, Shuyue; Liu, Yaping; Khan, Afsar; Li, Yanping; Cao, Jun; Cheng, Guiguang

doi:10.1016/j.jep.2021.114304

Cited by 39 publications

(27 citation statements)

References 38 publications

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“…Accumulated evidence has indicated that the intestinal barrier could prevent intestinal mucosal injury by blocking exogenous substances, and has played an essential role in maintaining intestinal health and host immune regulation [30,31]. Tight junction (TJ) proteins, the key part of the intestinal barrier, form a physical barrier to strengthen the protective function of the intestine and play an indispensable role in maintaining intestinal barrier function [32].…”

Section: Discussionmentioning

confidence: 99%

“…NF-κB is a nuclear transcription factor in cells and regulates the inflammatory response by modulating the transcription of inflammatory genes [18]. In an inflammatory environment, NF-κB p65 is phosphorylated and translocated into the nucleus, thereby promoting the transcription of inflammatory markers and inducing irreversible inflammatory injury, which is the important mechanism for regulating inflammatory diseases [31,32,41]. Additionally, the NF-κB pathway is also a crucial factor responsible for the disruption of the intestinal barrier and activation of NLRP3 inflammasome [36].…”

Section: Discussionmentioning

confidence: 99%

“…MAPK is a family of threonine/serine protein kinases. The activation of the MAPK pathway involves the phosphorylation of JNK, ERK and p38, which regulates the expression of inflammatory genes [31,42]. Importantly, the MAPK signaling pathway has been proved to regulate intestinal TJ proteins [24].…”

Section: Discussionmentioning

confidence: 99%

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Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Liu

Chi

Yang

et al. 2022

Toxins

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Staphylococcal enterotoxin A (SEA), the toxin protein secreted by Staphylococcus aureus, can cause staphylococcal food poisoning outbreaks and seriously threaten global public health. However, little is known about the pathogenesis of SEA in staphylococcal foodborne diseases. In this study, the effect of SEA on intestinal barrier injury and NLRP3 inflammasome activation was investigated by exposing BALB/c mice to SEA with increasing doses and a potential toxic mechanism was elucidated. Our findings suggested that SEA exposure provoked villi injury and suppressed the expression of ZO-1 and occludin proteins, thereby inducing intestinal barrier dysfunction and small intestinal injury in mice. Concurrently, SEA significantly up-regulated the expression of NLRP3 inflammasome-associated proteins and triggered the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways in jejunum tissues. Notably, selective inhibitors of MAPKs and NF-κB p65 ameliorated the activation of NLRP3 inflammasome stimulated by SEA, which further indicated that SEA could activate NLRP3 inflammasome through NF-κB/MAPK pathways. In summary, SEA was first confirmed to induce intestinal barrier dysfunction and activate NLRP3 inflammasome via NF-κB/MAPK signaling pathways. These findings will contribute to a more comprehensive understanding of the pathogenesis of SEA and related drug-screening for the treatment and prevention of bacteriotoxin-caused foodborne diseases via targeting specific pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Liu

Chi

Yang

et al. 2022

Toxins

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“…Ulcerative colitis can be ameliorated by inhibiting MAPK activation and mediating gut barrier integrity. 62 Therefore, it is speculated that MFD might have alleviated the LPS-induced increase in the phosphorylation of p38 MAPK and JNK, thus reducing colonic inflammation in offspring. LR can secrete reuterin and lactic acid to improve gut health and enhance immunity.…”

Section: Discussionmentioning

confidence: 99%

Maternal consumption of a fermented diet protects offspring against intestinal inflammation by regulating the gut microbiota

et al. 2022

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The neonatal intestinal tract is immature and can be easily infected by pathogens causing inflammation. Maternal diet manipulation is a promising nutritional strategy to enhance the gut health of offspring. A fermented diet is a gut microbiota targeting diet containing live probiotics and their metabolites, which benefit the gut and overall health host. However, it remains unclear how a maternal fermented diet (MFD) affects neonatal intestinal inflammation. Here, in vivo and in vitro models together with multi-omics analysis were applied to investigate the impacts and the underlying mechanism through which an MFD prevents from gut inflammation in neonates. An MFD remarkably improved the performance of both sows and piglets and significantly altered the gut microbiome and milk metabolome of sows. In addition, the MFD significantly accelerated the maturation of the gut microbiota of neonates and increased the abundance of gut Lactobacillus and the microbial functions of amino acid-related enzymes and glucose metabolism on the weaning day. Notably, the MFD reduced susceptibility to colonic inflammation in offspring. The fecal microbiota of sows was then transplanted into mouse dams and it was found that the mouse dams and pups in the MFD group alleviated the LPS-induced decrease in gut Lactobacillus abundance and barrier injury. Milk L-glutamine (GLN) and gut Lactobacillus reuteri (LR) were found as two of the main MFD-induced sow effectors that contributed to the gut health of piglets. The properties of LR and GLN in modulating gut microbiota and alleviating colonic inflammation by inhibiting the phosphorylation of p38 and JNK and activation of Caspase 3 were further verified. These findings provide the first data revealing that an MFD drives neonate gut microbiota development and ameliorates the colonic inflammation by regulating the gut microbiota. This fundamental evidence might provide references for modulating maternal nutrition to enhance early-life gut health and prevent gut inflammation.

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“…Previous studies have found that the TLR4 activation and the NF-κB translocating into the nucleus were two very important mechanisms for regulating inflammatory diseases [ 36 , 37 ]. The TLR4 activation can produce a large amount of myeloid differentiation primary response protein 88 (MyD88), which further activates the ubiquitin ligase TRAF6.…”

Section: Discussionmentioning

confidence: 99%

Ethanolic Extract from Pteris wallichiana Alleviates DSS-Induced Intestinal Inflammation and Intestinal Barrier Dysfunction by Inhibiting the TLR4/NF-κB Pathway and Regulating Tight Junction Proteins

et al. 2022

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The aim of the research was to determine the protective effect and mechanism of Pteris wallichiana J. Agardh extract (PWE) on DSS-induced ulcerative colitis (UC) in mice. In this research, PWE is rich in flavonoids and diterpenoids by UPLC-MS/MS analysis. In LPS-induced RAW264.7 cells, PWE reduced the productions of inflammatory factors (i.e., NO, TNF-α, IL-6, and IL-1β). In DSS-induced UC in mice, PWE improved disease activity index (DAI) score, attenuated oxidative stress by decreasing MPO and MDA activities and activating GSH and SOD levels, and inhibited TNF-α, IL-6, and IL-1β expressions in the colonic tissues. PWE also improved the intestinal barrier by upregulating the expressions of tight junction proteins, including occludin and ZO-1. Moreover, PWE extract alleviated intestinal inflammation by suppressing the TLR4/MyD88/NF-κB signaling pathway. Conclusion: PWE can alleviate DSS-induced UC in mice by increasing the expressions of intestinal tight junction proteins and inhibiting the TLR4/NF-κB inflammatory pathway.

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Anneslea fragrans Wall. ameliorates ulcerative colitis via inhibiting NF-κB and MAPK activation and mediating intestinal barrier integrity

Cited by 39 publications

References 38 publications

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Maternal consumption of a fermented diet protects offspring against intestinal inflammation by regulating the gut microbiota

Ethanolic Extract from Pteris wallichiana Alleviates DSS-Induced Intestinal Inflammation and Intestinal Barrier Dysfunction by Inhibiting the TLR4/NF-κB Pathway and Regulating Tight Junction Proteins

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