Opposite Effects of Interferon Regulatory Factor 1 and Osteopontin on the Apoptosis of Epithelial Cells Induced by TNF-α in Inflammatory Bowel Disease

Tang, Rui; Yang, Guang; Zhang, Shenghong; Wu, Changyou; Chen, Minhu

doi:10.1097/mib.0000000000000192

Cited by 38 publications

(32 citation statements)

References 40 publications

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“…Accumulating evidence has shown that decreased levels of TNF-α in the intestinal tissue and serum reduce IECs apoptosis in UC. [39] In line with this, in this study, we found that treatment with HNG significantly decreased caspase-3 activities compared to that in TNBS-treated rats. Therefore, we speculated that HNG prevented apoptosis caused by TNF-α in intestinal epithelial cells in UC.…”

Section: Discussionsupporting

confidence: 82%

Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats

Gültekin

Emre

Çelik

et al. 2017

Saudi J Gastroenterol

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Section: Discussionsupporting

confidence: 82%

Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats

Gültekin

Emre

Çelik

et al. 2017

Saudi J Gastroenterol

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“…Recently, elevated plasma levels were shown to be correlated with disease activity (Komine-Aizawa et al 2015). However, reduced expression of OPN in UC and CD as compared with normal controls was found in a cohort of Chinese patients (Tang et al 2014), although this difference may be explained by a focus on expression in epithelial rather than inflammatory cells. Interestingly, a haplotype consisting of 8 single-nucleotide polymorphisms in the OPN gene was found to exhibit significant associations with CD susceptibility (Glas et al 2011), further supporting an association of OPN with this disease.…”

Section: Opn In Inflammatory Bowel Diseasesmentioning

confidence: 99%

Osteopontin in Immune-mediated Diseases

Rittling

Singh²

2015

J Dent Res

148

109

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Since its initial identification as one of the genes most highly upregulated upon T-cell activation, osteopontin (or Eta-1, as it was designated then) has been demonstrated to have many roles in the regulation of the immune response on multiple levels. It contributes to the development of immune-mediated and inflammatory diseases, and it regulates the host response to infection. In some cases, the mechanisms of these effects have been elucidated, while other mechanistic functions of the protein remain obscure. The protein itself makes these analyses complex, since it binds to a series of different integrins, and in addition to its classically secreted form, an intracellular form of osteopontin has been identified, which participates in several aspects of immune regulation. In this review, we focus on the role of osteopontin in a series of immune-related diseases, particularly those where significant advances have been made in recent years: multiple sclerosis, rheumatoid arthritis, lupus and related diseases, Sjögren's disease, colitis, and 1 area of inflammatory pathology, alcoholic and nonalcoholic liver diseases. A recurring theme in these diseases is a link between osteopontin and pathogenic T cells, particularly T helper 17 cells, where osteopontin produced by dendritic cells supports IL-17 expression, contributing to pathology. In addition, a role for osteopontin in B-cell differentiation is becoming clear. In general, osteopontin contributes to pathology in these diseases, but there are examples where it has a protective role; deciphering the mechanisms underlying these differences and the specific receptors for osteopontin will be a research challenge for the future. Aside from its newly discovered role in the development of Sjögren's disease, the role of osteopontin in inflammatory conditions in the oral cavity is still poorly understood. Elucidation of this role will be of interest.

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“…In addition to IBD, other inflammatory processes may condition intestinal homeostasis, such as food allergies. Compelling evidence during the past decade have demonstrated that T cell-mediated mechanisms promote mucosal inflammation in IBD (Neurath et al, 2001;Sturm et al, 2008;Gerner et al, 2013) and dramatically compromise the epithelial cell compartment (Siggers & Hackam, 2011;Planell et al, 2012;Tang et al, 2014;Thagia et al, 2014).…”

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confidence: 99%

Inflammation Controls Sensitivity of Human and Mouse Intestinal Epithelial Cells to Galectin-1

et al. 2015

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Galectins play key roles in the inflammatory cascade. In this study, we aimed to analyze the effect of galectin-1 (Gal-1) in the function of intestinal epithelial cells (IECs) isolated from healthy and inflamed mucosa. IECs isolated from mice or patients with inflammatory bowel diseases (IBD) were incubated with different pro-inflammatory cytokines, and Gal-1 binding, secretion of homeostatic factors and viability were assessed. Experimental models of food allergy and colitis were used to evaluate the in vivo influence of inflammation on Gal-1 binding and modulation of IECs. We found an enhanced binding of Gal-1 to: (a) murine IECs exposed to IL-1β, TNF, and IL-13; (b) IECs from inflamed areas in intestinal tissue from IBD patients; (c) small bowel of allergic mice; and (d) colon from mice with experimental colitis. Our results showed that low concentrations of Gal-1 favored a tolerogenic micro-environment, whereas high concentrations of this lectin modulated viability of IECs through mechanisms involving activation of caspase-9 and modulation of Bcl-2 protein family members. Our results showed that, when added in the presence of diverse pro-inflammatory cytokines such as tumor necrosis factor (TNF), IL-13 and IL-5, Gal-1 differentially promoted the secretion of growth factors including thymic stromal lymphopoietin (TSLP), epidermal growth factor (EGF), IL-10, IL-25, and transforming growth factor (TGF-β1 ). In conclusion, we found an augmented binding of Gal-1 to IECs when exposed in vitro or in vivo to inflammatory stimuli, showing different effects depending on Gal-1 concentration. These findings highlight the importance of the inflammatory micro-environment of mucosal tissues in modulating IECs susceptibility to the immunoregulatory lectin Gal-1 and its role in epithelial cell homeostasis.

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Opposite Effects of Interferon Regulatory Factor 1 and Osteopontin on the Apoptosis of Epithelial Cells Induced by TNF-α in Inflammatory Bowel Disease

Abstract: Our data suggest that during intestinal inflammation, the TNF-α-mediated activation of IRF1 is related to the subsequent suppression of OPN expression, further reducing p-AKT, p-P38, and p-ERK activities and resulting in aggravation of the injury to intestinal epithelial cells.

Cited by 38 publications

References 40 publications

Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats

Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats

Osteopontin in Immune-mediated Diseases

Inflammation Controls Sensitivity of Human and Mouse Intestinal Epithelial Cells to Galectin-1

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