Sodium butyrate inhibits the NF-kappa B signaling pathway and histone deacetylation, and attenuates experimental colitis in an IL-10 independent manner

Lee, Changhyun; Kim, Byeong Gwan; Kim, Jee Hyun; Chun, Jaeyoung; Im, Jong Pil; Kim, Sang Woo

doi:10.1016/j.intimp.2017.07.023

Cited by 183 publications

(134 citation statements)

References 43 publications

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“…Subsequent treatments were given daily throughout the entire experiment. The dose and route of I3C is consistent with our previous reports (14,18), and the NaB dosage and route were determined based on other published reports (27)(28)(29)85). All experimental groups in the TNBS model were given 50% ethanol intrarectal injections to ensure changes observed were not due to administration of the ethanol diluent.…”

Section: Methodsmentioning

confidence: 80%

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Busbee¹,

Menzel²,

Alrafas³

et al. 2020

JCI Insight

102

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Section: Methodsmentioning

confidence: 80%

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Busbee¹,

Menzel²,

Alrafas³

et al. 2020

JCI Insight

102

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“…Similarly, butyrate suppressed the cytokine-induced expression of ICAM-1 in primary oral epithelial cells ( Figure 2). Then, and in order to validate these observations, we used another experimental setting using primary mouse macrophages [37][38][39]. Notably, butyrate was capable of inhibiting the LPS-and saliva-induced ICAM-1 expression in primary mouse macrophages ( Figure 3).…”

Section: Butyrate But Not Acetate and Propionate Decrease The Expressmentioning

confidence: 94%

Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells

Magrin

Summa

Strauß

et al. 2020

IJMS

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Short-chain fatty acids (SCFA) are bacterial metabolites that can be found in periodontal pockets. The expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) within the epithelium pocket is considered to be a key event for the selective transmigration of leucocytes towards the gingival sulcus. However, the impact of SCFA on ICAM-1 expression by oral epithelial cells remains unclear. We therefore exposed the oral squamous carcinoma cell line HSC-2, primary oral epithelial cells and human gingival fibroblasts to SCFA, namely acetate, propionate and butyrate, and stimulated with known inducers of ICAM-1 such as interleukin-1-beta (IL1β) and tumor necrosis factor-alfa (TNFα). We report here that butyrate but not acetate or propionate significantly suppressed the cytokine-induced ICAM-1 expression in HSC-2 epithelial cells and primary epithelial cells. The G-protein coupled receptor-43 (GPR43/ FFAR2) agonist but not the histone deacetylase inhibitor, trichostatin A, mimicked the butyrate effects. Butyrate also attenuated the nuclear translocation of p65 into the nucleus on HSC-2 cells. The decrease of ICAM-1 was independent of Nrf2/HO-1 signaling and phosphorylation of JNK and p38. Nevertheless, butyrate could not reverse an ongoing cytokine-induced ICAM-1 expression in HSC-2 cells. Overall, these observations suggest that butyrate can attenuate cytokine-induced ICAM-1 expression in cells with epithelial origin.Int. J. Mol. Sci. 2020, 21, 1679 2 of 15 crevicular fluid by means of a tightly controlled expression of adhesion molecules, thereby defending microbiological antagonism in the periodontal tissue [2,3]. Thus, the increase of adhesion molecules by inflammatory mediators has to be counterbalanced by local cues to control an excessive influx of cells of the innate immune system.The influx of cells is controlled by intercellular adhesion molecule-1 (ICAM-1), allowing the transmigration of leucocytes which express the corresponding lymphocyte function-associated antigen-1 and macrophage adhesion ligand-1 [4]. ICAM-1, being induced by inflammatory cues such as interleukin-1-beta (IL1β) and tumor necrosis factor-α (TNFα) [5], is expressed by the vascular endothelium and by the junctional epithelium [6], thus, facilitating transmigration of leukocytes across vascular endothelia and the invasion of the extracellular matrix [7]. Although ICAM-1 is consistently expressed by junctional epithelial cells in healthy gingiva and in pocket epithelium, it is not detectable on the majority of keratinocytes in the external gingival epithelium [6,8]. The question then arises, how is the expression of ICAM-1 in epithelial cells controlled?The increase of ICAM-1 expression by inflammatory cues is evidently well-documented. Inflammatory mediators including IL-6 and prostaglandin E 2 increase ICAM-1 expression in human oral squamous cell carcinoma SCC4 cells in vitro [9,10]. Primary gingival epithelial cells increasingly express ICAM-1 upon inflammatory cytokines stimuli, namely, TNFα and interferon-γ [11]....

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“…Various omic technologies (like genomics, proteomics, metabolomics and metatranscriptomics), together with developments in bioinformatics over the last decade have helped us realize the beneficial effects of gut bacteria on human health or ‘gut symbiosis’ ( Figure ). We now know that gut microbes help metabolize several important food constituents ( Table ) . For example, non‐digestible fibres in the diet (like plant cell‐wall polysaccharides and resistant starches) are metabolized by healthy anaerobic gut bacteria to short‐chain fatty acids (SCFA) .…”

Section: Gut Microbes and Symbiosismentioning

confidence: 99%

“…For example, non‐digestible fibres in the diet (like plant cell‐wall polysaccharides and resistant starches) are metabolized by healthy anaerobic gut bacteria to short‐chain fatty acids (SCFA) . SCFA butyrate acts as an energy source for colonocytes, plays an important role in maintaining intestinal wall integrity by facilitating ‘tight junction’ assembly and can have important immune regulatory functions by inhibiting nuclear factor‐kappa B (NF‐κB) signalling and by inducing the differentiation of colonic regulatory T cells . Other SCFAs like acetate and propionate can affect several organ systems outside the gastrointestinal tract by binding to free fatty acid receptors (FFAR 2/3) on a variety of cells in the body including the immune system, enteroendocrine tissue and even neurons in the sympathetic ganglia and autonomic nervous system .…”

Section: Gut Microbes and Symbiosismentioning

confidence: 99%

Gut dysbiosis and heart failure: navigating the universe within

Madan

Mehra

2020

European J of Heart Fail

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Alternations in gut microbial composition (i.e. loss of microbial diversity or ‘gut dysbiosis’) have been associated with heart failure with reduced ejection fraction (HFrEF). It has also been suggested that increased chronic low‐level inflammation and immune system dysregulation seen in patients with HFrEF could be related to gut dysbiosis and increased intestinal permeability. Hence, the concept of modulating gut microbial composition with the goal of reducing systemic inflammation and controlling HFrEF progression has generated a substantial interest in the scientific community. However, several challenges to the gut dysbiosis theory remain as the exact gut microbial composition in HFrEF patients in these studies is not the same and a common microbiome linked to HFrEF is not yet established. With the advances in culture independent sequencing techniques it has also become evident that the gut microbiome may be much more diverse than previously believed. Further, various ‘omic’ technologies have enabled us to appreciate the potential role of gut microbial metabolites in various physiological processes in the host. Hence, identification of specific gut microbial metabolites may offer an alternative approach at solving this gut microbiome‐HFrEF puzzle. In the current review, we evaluate the concept of gut symbiosis, the potential role of gut dysbiosis in systemic inflammation and HFrEF, and finally highlight the challenges faced by the gut dysbiosis theory in HFrEF and provide a framework for the possible solutions.

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Sodium butyrate inhibits the NF-kappa B signaling pathway and histone deacetylation, and attenuates experimental colitis in an IL-10 independent manner

Cited by 183 publications

References 43 publications

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells

Gut dysbiosis and heart failure: navigating the universe within

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