HMGB1 exacerbates experimental mouse colitis by enhancing innate lymphoid cells 3 inflammatory responses via promoted IL-23 production

Chen, Xiangyu; Li, Lingyun; Khan, Muhammad Noman; Shi, Lifeng; Wang, Zhongyan; Zheng, Fang; Gong, Feili; Fang, Min

doi:10.1177/1753425916669862

Cited by 30 publications

(16 citation statements)

References 39 publications

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“…Previous studies showed elevated HMGB1 levels in the stools of IBD patients . Moreover, studies showed that inhibition of HMGB1 significantly ameliorated experimentally induced colitis in mice . In our study, the disease group was found to exhibit significantly elevated HMGB1 mRNA transcripts compared with the control group, which indicates significant inflammation and a subsequent increase in HMGB1 expression.…”

Section: Discussionsupporting

confidence: 63%

The natural flavonoid galangin ameliorates dextran sulphate sodium–induced ulcerative colitis in mice: Effect on Toll‐like receptor 4, inflammation and oxidative stress

Gerges

Tolba

Elsherbiny

et al. 2020

Basic Clin Pharma Tox

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This study was carried out to investigate the potential therapeutic effect of galangin, a promising active principle of honeybee propolis, in dextran sulphate sodium (DSS)–induced colitis in mice. We explored the possible underlying mechanisms for galangin action and the therapeutic benefit of adding galangin to the standard therapy sulphasalazine. A galangin dose of 40 mg/kg was selected based on a preliminary dose‐selection study for investigation in a 4‐week cyclical model of DSS‐induced colitis. Mice received 3% DSS in their drinking water during the first and third weeks and were administered the treatments (40 mg/kg galangin, 100 mg/kg sulphasalazine and a combination of 20 mg/kg galangin and 50 mg/kg sulphasalazine) daily starting from the second week. Galangin significantly ameliorated DSS‐induced histopathological alterations and tissue injury, down‐regulated Toll‐like receptor 4 expression, suppressed NF‐κB p65 activation, lowered inflammatory cytokine levels and demonstrated antioxidant effects. The combination of galangin and sulphasalazine at half doses yielded comparable results to either drug alone at full dose. This study highlights galangin as a promising therapy for colitis management.

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Section: Discussionsupporting

confidence: 63%

The natural flavonoid galangin ameliorates dextran sulphate sodium–induced ulcerative colitis in mice: Effect on Toll‐like receptor 4, inflammation and oxidative stress

Gerges

Tolba

Elsherbiny

et al. 2020

Basic Clin Pharma Tox

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“…Subsequently, samples of colon tissues were prepared for tissue sections, and then stained with hematoxylin and eosin. Histological analysis was performed as described in previous report [13].…”

Section: Methodsmentioning

confidence: 99%

IL-33 ameliorates experimental colitis involving regulation of autophagy of macrophages in mice

et al. 2019

Self Cite

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BackgroundPreviously, we have demonstrated that IL-33 administration protecting TNBS-induced experimental colitis is associated with facilitation of Th2/Tregs responses in mice. However, whether IL-33 regulates autophagy to ameliorate experimental colitis is unclear.ResultsIL-33 administration (2 μg/day, intraperitoneal injection), while facilitating Th2/Tregs responses, also enhances the autophagy in mice with TNBS-induced colitis as well as macrophages. In the meantime, we observed that inhibition of the autophagy with 3-methyladenine (3-MA) (24 mg/kg, intraperitoneal injection) in mice exacerbates TNBS-induced experimental colitis. On the contrary, administration of rapamycin (2 mg/kg,intragastric administration), an autophagy-enhancer, alleviates the colitis in mice. In vivo, Immunofluorescence analysis revealed that TNBS combined with IL-33 enhanced the autophagy of macrophages in the inflammatory gut tissue. In vitro, treatment with IL-33 promoted the autophagy of macrophages generated from bone marrow cells in dose-dependant manner. Furthermore, the effect of autophagy-enhancement by IL-33 is TLR4 signaling pathway dependant. Our notion was further confirmed by IL-33-deficient bone marrow-derived macrophages cells.ConclusionsIL-33 regulates the autophagy is a new immunoregulatory property on TNBS-induced experimental colitis in mice.

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“…Specific antibody therapies against these targets seem to be effective in most cases but very expensive [11]. Furthermore, nuclear mediators, such as NF-κB and high mobility group binding 1 (HMGB1), are also important in IBD as proinflammatory stimuli [12,13]. HMGB1 is suggested as a potential biomarker in IBD patients' feces [14], while anti-HMGB-1 therapy seems to be promising in a mouse model of colitis [13].…”

Section: Introductionmentioning

confidence: 99%

Lessons on the Sigma-1 Receptor in TNBS-Induced Rat Colitis: Modulation of the UCHL-1, IL-6 Pathway

Almási

Török

Dvorácskó

et al. 2020

IJMS

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Inflammatory Bowel Disease (IBD) is an autoimmune ailment of the gastrointestinal (GI) tract, which is characterized by enhanced activation of proinflammatory cytokines. It is suggested that the sigma-1 receptor (σ1R) confers anti-inflammatory effects. As the exact pathogenesis of IBD is still unknown and treatment options are limited, we aimed to investigate the effects of σ1R in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis. To this end, male Wistar–Harlan rats were used to model colitic inflammation through the administration of TNBS. To investigate the effects of σ1R, Fluvoxamine (FLV, σ1R agonist) and BD1063 (σ1R antagonist) were applied via intracolonic administration to the animals once a day for three days. Our radioligand binding studies indicated the existence of σ1Rs as [3H](+)-pentazocine binding sites, and FLV treatment increased the reduced σ1R maximum binding capacity in TNBS-induced colitis. Furthermore, FLV significantly attenuated the colonic damage, the effect of which was abolished by the administration of BD1063. Additionally, FLV potentially increased the expression of ubiquitin C-terminal hydrolase ligase-1 (UCHL-1) and the levels of endothelial nitric oxide synthase (eNOS), and decreased the levels of interleukin-6 (IL-6) and inducible NOS (iNOS) expression. In summary, our study offers evidence for the anti-inflammatory potential of FLV and σ1R in experimental colitis, and our results present a promising approach to the development of new σ1R-targeted treatment options against IBD.

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HMGB1 exacerbates experimental mouse colitis by enhancing innate lymphoid cells 3 inflammatory responses via promoted IL-23 production

Cited by 30 publications

References 39 publications

The natural flavonoid galangin ameliorates dextran sulphate sodium–induced ulcerative colitis in mice: Effect on Toll‐like receptor 4, inflammation and oxidative stress

The natural flavonoid galangin ameliorates dextran sulphate sodium–induced ulcerative colitis in mice: Effect on Toll‐like receptor 4, inflammation and oxidative stress

IL-33 ameliorates experimental colitis involving regulation of autophagy of macrophages in mice

Lessons on the Sigma-1 Receptor in TNBS-Induced Rat Colitis: Modulation of the UCHL-1, IL-6 Pathway

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