The rationale for selenium supplementation in inflammatory bowel disease: A mechanism-based point of view

Ala, Moein; Kheyri, Zahedin

doi:10.1016/j.nut.2021.111153

Cited by 44 publications

(18 citation statements)

References 157 publications

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“…The endogenous antioxidant system such as SOD, CAT, and GR can reduce oxidative stress and ROS production directly or indirectly. It is widely recognized that selenoproteins exert an antioxidant effect by participating in the synthesis of antioxidant enzymes (Ala and Kheyri, 2021). In the present study, the results showed that the content of MDA was significantly increased after DSS administration.…”

Section: Discussionsupporting

confidence: 57%

“…Probiotics such as Lactobacillus and Bifidobacterium are safe and proven effective in the treatment of UC by mediating microbiota dysbiosis, enhancing intestinal integrity and generating functional metabolites (Sanders et al, 2019). Additionally, as an essential trace element, selenium, especially the organic selenium, is famous for its antioxidative properties and effect on regulating immune systems, thus playing a positive role in UC treatment (Ala and Kheyri, 2021). In this report, we found that Se-B.…”

Section: Discussionmentioning

confidence: 72%

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Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

Jin

Gao

et al. 2022

Front. Microbiol.

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The pathogenesis of ulcerative colitis (UC) is complicated with impaired intestinal epithelial barrier and imbalanced gut microbiota. Both selenium and probiotics have shown effects in regulating intestinal flora and ameliorating UC. The objective of this study is to investigate the alleviating effects of Selenium-enriched Bifidobacterium longum DD98 (Se-B. longum DD98) on dextran sulfate sodium (DSS)-induced colitis in mice and explore the underlying mechanism. After treatment of B. longum DD98, Se-B. longum DD98, and sulfasalazine for 3 weeks, the disease severity of UC mice was decreased, with colon lengthened and pathological phenotype improved. The expression of pro-inflammatory cytokines and oxidative stress parameters were also decreased. Thus, Se-B. longum DD98 showed a stronger effect on relieving the aforementioned symptoms caused by DSS-induced colitis. Exploration of the potential mechanism demonstrated that Se-B. longum DD98 showed higher activities to suppress the inflammatory response by inhibiting the activation of the toll-like receptor 4 (TLR4), compared to B. longum DD98 and sulfasalazine. Se-B. longum DD98 also significantly improved the intestinal barrier integrity by increasing the expression of tight junction proteins including ZO-1 and occludin. 16S rDNA sequencing analyses showed that Se-B. longum DD98 improved the diversity of the intestinal flora and promoted the abundance of health-benefiting taxa including Lachnospiraceae, Lactobacillaceae, and Prevotellaceae in family level. In conclusion, compared to B. longum DD98 and sulfasalazine, Se-B. longum DD98 showed stronger therapeutic effects on DSS-induced colitis in mice and might be a promising candidate for the treatment of UC.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 72%

Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

Jin

Gao

et al. 2022

Front. Microbiol.

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“…A similar study also investigated the effect of nonmetal-based nanomaterials on macrophage polarization by using selenium (Se) ( Zhu et al, 2017 ). Se is an indispensable nutrient and its deceased level may be associated with the exacerbation of IBD ( Castro Aguilar-Tablada et al, 2016 ; Zhu et al, 2017 ; Ala and Kheyri, 2021 ). SeNPs have anti-inflammatory activity and low toxicity.…”

Section: Targeting Macrophages For Ibdmentioning

confidence: 99%

The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease

Zhang

Liu

et al. 2022

Front. Cell Dev. Biol.

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Inflammatory bowel disease (IBD), comprising Crohn’s disease and ulcerative colitis, is a refractory disease with many immune abnormalities and pathologies in the gastrointestinal tract. Because macrophages can distinguish innocuous antigens from potential pathogens to maintain mucosa barrier functions, they are essential cells in the intestinal immune system. With numerous numbers in the intestinal tract, tissue-resident macrophages have a signiﬁcant effect on the constant regeneration of intestinal epithelial cells and maintaining the immune homeostasis of the intestinal mucosa. They also have a significant influence on IBD through regulating pro-(M1) or anti-inﬂammatory (M2) phenotype polarization according to different environmental cues. The disequilibrium of the phenotypes and functions of macrophages, disturbed by intracellular or extracellular stimuli, influences the progression of disease. Further investigation of macrophages’ role in the progression of IBD will facilitate deciphering the pathogenesis of disease and exploring novel targets to develop novel medications. In this review, we shed light on the origin and maintenance of intestinal macrophages, as well as the role of macrophages in the occurrence and development of IBD. In addition, we summarize the interaction between gut microbiota and intestinal macrophages, and the role of the macrophage-derived exosome. Furthermore, we discuss the molecular and cellular mechanisms participating in the polarization and functions of gut macrophages, the potential targeted strategies, and current clinical trials for IBD.

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“…Similarly, it was found that selenium alone or in combination with other substances such as vitamin E mitigates the intensity of damage due to its anti-oxidant properties [19][20][21]. Furthermore, selenium supports gut commensal microbiota and enhances their protective effects on intestinal lining [21].…”

Section: Introductionmentioning

confidence: 97%

Sodium Selenite Modulates IDO1/Kynurenine, TLR4, NF-κB and Bcl2/Bax  Pathway and Mitigates Acetic Acid-Induced Colitis in Rat

2022

Cell Physiol Biochem

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BACKGROUND/AIMS: Colitis is a main presentation of inflammatory bowel disease (IBD) and yet, has no definitive cure. Currently, corticosteroids, anti-tumor necrosis factor (anti-TNF) agents and 5-aminosalicylic acid derivatives are prescribed for management of colitis. Except their failure rate, they are not always tolerated because of their severe adverse effects. Additive formulas with fewer adverse effects may improve the treatment of colitis. METHODS: In this study, colitis was induced with intra-rectal injection of three concentrations of acetic acid (4, 6 and 8 v/v). Each group received sodium selenite (0.5 mg/kg) or saline, gavaged on days 0 and 1 for treatment. Two days after induction of colitis, rats were sacrificed and the end part of their colons were resected for macroscopic and microscopic evaluation and molecular measurement. RESULTS: Sodium selenite improved macroscopic and microscopic view of the colon, decreased cryptitis, crypt abscess and inflammatory cells infiltration and partly maintained mucosal structure. Sodium selenite markedly reduced tissue levels of malondialdehyde (MDA), TNF-α and interferon γ (INF-γ) and decreased myeloperoxidase (MPO) activity. Treatment with sodium selenite also significantly downregulated IL17, IL22, indoleamine 2,3-dioxygenase (IDO1), and kynurenine levels. Western blotting revealed that sodium selenite prevented apoptosis by increasing bcl2/Bax ratio. Furthermore, our findings showed that sodium selenite significantly downregulated the upstream inflammatory molecules such as nuclear factor kappa B (NF-κB) and toll-like receptor 4 (TLR4) in colitis. CONCLUSION: These findings show that sodium selenite alleviates inflammatory response and oxidative stress and protects against colitis.

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The rationale for selenium supplementation in inflammatory bowel disease: A mechanism-based point of view

Cited by 44 publications

References 157 publications

Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease

Sodium Selenite Modulates IDO1/Kynurenine, TLR4, NF-κB and Bcl2/Bax  Pathway and Mitigates Acetic Acid-Induced Colitis in Rat

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The rationale for selenium supplementation in inflammatory bowel disease: A mechanism-based point of view

Cited by 44 publications

References 157 publications

Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease

Sodium Selenite Modulates IDO1/Kynurenine, TLR4, NF-κB and Bcl2/Bax Pathway and Mitigates Acetic Acid-Induced Colitis in Rat

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Sodium Selenite Modulates IDO1/Kynurenine, TLR4, NF-κB and Bcl2/Bax  Pathway and Mitigates Acetic Acid-Induced Colitis in Rat