Amelioration of dextran sulfate colitis by butyrate: role of heat shock  protein 70 and NF-κB

Venkatraman, Aparna; Ramakrishna, Banumathi; Shaji, R. V.; Kumar, Navalpur S. Nanda; Pulimood, Anna; Patra, Susama

doi:10.1152/ajpgi.00307.2002

Cited by 121 publications

(84 citation statements)

References 48 publications

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“…In previous studies, it was shown that butyrate can inhibit the binding of NF-B to DNA (12,15,47). In contrast, in the reporter gene assays, butyrate enhanced the transcriptional activity driven by NF-B sites and the TNF␣ promoter in a dose-dependent manner ( Figures 3A and B).…”

Section: Discussionmentioning

confidence: 74%

Butyrate suppresses tumor necrosis factor α production by regulating specific messenger RNA degradation mediated through acis-acting AU-rich element

Fukae¹,

Amasaki²,

Yamashita³

et al. 2005

Arthritis Rheum

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Objective. To study the capacity of butyrate to inhibit production of tumor necrosis factor ␣ (TNF␣) in macrophage-like synoviocytes (MLS) from patients with rheumatoid arthritis (RA), in human peripheral monocytes, and in murine RAW264.7 macrophages.Methods. The concentrations of TNF␣ in culture supernatants of these cells were measured using enzyme-linked immunosorbent assay. The expression levels of various messenger RNAs (mRNA), such as those for TNF␣, the mRNA-binding protein TIS11B, and luciferase, were measured using real-time quantitative polymerase chain reaction. The in vitro effects of butyrate on transcriptional regulation were evaluated by transfection with various reporter plasmids in RAW264.7 macrophages. The effects of TIS11B on TNF␣ expression were examined using an overexpression model of TIS11B in RAW264.7 cells.Results. Butyrate suppressed TNF␣ protein and mRNA production in MLS and monocytes, but paradoxically enhanced transactivation of the TNF␣ promoter. Expression of the AU-rich element (ARE)-binding protein TIS11B was up-regulated by butyrate. Induction of TNF␣ mRNA by lipopolysaccharide was significantly inhibited when TIS11B was overexpressed. Butyrate facilitated the degradation of luciferase transcripts containing the 3-untranslated region (3-UTR) of TNF␣, and this effect was dependent on the ARE in the 3-UTR that is known to be involved in the regulation of mRNA degradation.Conclusion. These results indicate that butyrate suppresses TNF␣ expression by facilitating mRNA degradation mediated through a cis-acting ARE. Butyrate has the ability to regulate TNF␣ at the mRNA level and is therefore a potential therapeutic drug for RA patients.

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Section: Discussionmentioning

confidence: 74%

Butyrate suppresses tumor necrosis factor α production by regulating specific messenger RNA degradation mediated through acis-acting AU-rich element

Fukae¹,

Amasaki²,

Yamashita³

et al. 2005

Arthritis Rheum

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“…Because some HSPs have been reported to be overexpressed in the intestinal tissues of IBD patients (19,20,23) and in an animal model of IBD (21)(22)(23). HSF1 and HSPs are thought to be involved in the pathogenesis of IBD.…”

Section: Discussionmentioning

confidence: 99%

Genetic Evidence for a Protective Role for Heat Shock Factor 1 and Heat Shock Protein 70 against Colitis

Tanaka

Namba

Arai

et al. 2007

Journal of Biological Chemistry

130

126

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Inflammatory bowel disease (IBD) involves infiltration of leukocytes into intestinal tissue, resulting in intestinal damage induced by reactive oxygen species (ROS). Pro-inflammatory cytokines and cell adhesion molecules (CAMs) play important roles in this infiltration of leukocytes. The roles of heat shock factor 1 (HSF1) and heat shock proteins (HSPs) in the development of IBD are unclear. In this study, we examined the roles of HSF1 and HSPs in an animal model of IBD, dextran sulfate sodium (DSS)-induced colitis. The colitis worsened or was ameliorated in HSF1-null mice or transgenic mice expressing HSP70 (or HSF1), respectively. Administration of DSS up-regulated the expression of HSP70 in colonic tissues in an HSF1-dependent manner. Expression of pro-inflammatory cytokines and CAMs and the level of cell death observed in colonic tissues were increased or decreased in DSS-treated HSF1-null mice or transgenic mice expressing HSP70, respectively, relative to control wild-type mice. Relative to macrophages from control wildtype mice, macrophages prepared from HSF1-null mice or transgenic mice expressing HSP70 displayed enhanced or reduced activity, respectively, for the generation of pro-inflammatory cytokines in response to lipopolysaccharide stimulation. Suppression of HSF1 or HSP70 expression in vitro stimulated lipopolysaccharide-induced up-regulation of CAMs or ROS-induced cell death, respectively. This study provides the first genetic evidence that HSF1 and HSP70 play a role in protecting against DSS-induced colitis. Furthermore, this protective role seems to involve various mechanisms, such as suppression of expression of pro-inflammatory cytokines and CAMs and ROS-induced cell death. Inflammatory bowel disease (IBD),2 Crohn disease, and ulcerative colitis have become substantial health problems with an actual prevalence of 200 -500 cases/100,000 people in western countries, which almost double every 10 years (1). Although the etiology of IBD is not yet fully understood, recent studies suggest that IBD involves chronic inflammatory disorders in the intestine because of "a vicious cycle." Infiltration into intestinal tissues causes intestinal mucosal damage induced by reactive oxygen species (ROS) that are released from the activated leukocytes, and this intestinal mucosal damage further stimulates the infiltration of leukocytes (2). To understand the molecular mechanism underlying the pathogenesis of IBD and to develop new types of clinical drugs for IBD, identification of endogenous factors that positively or negatively affect the development of IBD is important. For this purpose, various experimental animal colitis models, in particular the dextran sulfate sodium (DSS)-and trinitrobenzenesulfonic acid-induced colitis models, have been used (3).Pro-inflammatory cytokines play an important role in the activation and infiltration of leukocytes that are associated with IBD. This conclusion is supported by a range of evidence. Increases in the levels of various pro-inflammatory cytokines (such as tumor necr...

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“…The production of these pro-inflammatory cytokines is mediated mainly by transcriptional activation of nuclear factor κB (NF-κB) and mitogen activated protein kinase (MAPK) pathways (Malago et al, 2002;Ke et al, 2013). Several therapeutic interventions such as butyrate enemas modulate the activation of these pathways and suppress the production of pro-inflammatory cytokines to protect the colon against inflammatory injury (Venkatraman et al, 2003;Malago et al, 2005;Ke et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Intraperitoneal administration of butyrate prevents the severity of acetic acid colitis in rats

Malago

Sangu²

2015

J. Zhejiang Univ. Sci. B

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Intrarectal infusion of butyrate improves colorectal disorders including ulcerative colitis (UC). However, it is not established whether systemically administered butyrate benefits such patients. The current study aimed at exploring and comparing the potential of intraperitoneally, intrarectally, and orally administered butyrate against acetic acid (AA)-induced UC in rats. Intrarectal administration of 2 ml of 50% AA was done after or without prior treatment of rats for 7 consecutive days with 100 mg/kg sodium butyrate (SB) intraperitoneally, intrarectally, or orally. Rats were sacrificed after 48 h of AA-treatment. Subsequently, colon sections were processed routinely for histopathological examination. We clinically observed diarrhea, loose stools, and hemoccult-positive stools, and histologically, epithelial loss and ulceration, crypt damage, goblet cell depletion, hemorrhage, and mucosal infiltration of inflammatory cells. The changes were significantly reduced by intraperitoneal, intrarectal, or oral butyrate, with intraperitoneal butyrate exhibiting the highest potency. It is concluded that intraperitoneal administration of butyrate abrogates the lesions of AA-induced UC and its potency surpasses that of intrarectal or oral butyrate.

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Amelioration of dextran sulfate colitis by butyrate: role of heat shock protein 70 and NF-κB

Cited by 121 publications

References 48 publications

Butyrate suppresses tumor necrosis factor α production by regulating specific messenger RNA degradation mediated through acis-acting AU-rich element

Butyrate suppresses tumor necrosis factor α production by regulating specific messenger RNA degradation mediated through acis-acting AU-rich element

Genetic Evidence for a Protective Role for Heat Shock Factor 1 and Heat Shock Protein 70 against Colitis

Intraperitoneal administration of butyrate prevents the severity of acetic acid colitis in rats

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