Short-Chain Fatty Acids Inhibit Oxidative Stress and Inflammation in Mesangial Cells Induced by High Glucose and Lipopolysaccharide

Huang, Wei; Guo, Hengli; Deng, Xian; Zhu, Tingting; Xiong, Jianfeng; Xu, Youhua

doi:10.1055/s-0042-121493

Cited by 144 publications

(94 citation statements)

References 21 publications

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“…Nevertheless, further research is required to elucidate the precise role of butyrate in the periodontal tissues under different in vitro conditions. Our research supports the role of butyrate to reduce ICAM-1 expression as observed in the intestine of burned rats [40], stimulated chondrocytes [41], glomerular mesangial cells [42], colon cancer cells [43], and endothelial cells [44]. These observations together with our findings are, however, in contrast to those showing that butyrate increases ICAM-1 in gingival carcinoma cells [23,45], leukemia cells [46] and endothelial cells [47,48].…”

Section: Discussionsupporting

confidence: 89%

“…However, with respect to the beneficial effects of butyrate on colitis [33,34], pathological bone loss [35], anti-microbial activity [36], and on a M1-to-M2 shift in macrophages [37-39] it should not be ruled out that SCFA may also contribute to tissue homeostasis by modulation of ICAM-1.Butyrate markedly reduces ICAM-1 expression in the intestine of severely burned rats [40] and in IL1β-stimulated chondrocytes [41]. Butyrate also reduces the expression of ICAM-1 in LPS-stimulated mouse glomerular mesangial and Caco-2 cells [42,43], and cytokine-induced ICAM-1 expression in cultured endothelial cells [44]. Conversely, other studies showed that butyrate increases ICAM-1 in human gingival carcinoma cell line 45], in acute myeloid leukemia cells [46] and endothelial cells [47,48].…”

mentioning

confidence: 99%

“…Butyrate markedly reduces ICAM-1 expression in the intestine of severely burned rats [40] and in IL1β-stimulated chondrocytes [41]. Butyrate also reduces the expression of ICAM-1 in LPS-stimulated mouse glomerular mesangial and Caco-2 cells [42,43], and cytokine-induced ICAM-1 expression in cultured endothelial cells [44]. Conversely, other studies showed that butyrate increases ICAM-1 in human gingival carcinoma cell line 45], in acute myeloid leukemia cells [46] and endothelial cells [47,48].…”

mentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

mentioning

confidence: 99%

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

Magrin

Summa

Strauß

et al. 2020

IJMS

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“…The present study has also shown that the expression of STRs and associated signaling components (Gα-gustducin, PLCβ2, and TRPM5) was rapidly downregulated upon exposure to glucose in a timeand dose-dependent manner in vitro. GMC proliferation and hypertrophy, ECM accumulation, as well as consequent renal fibrosis induced by high glucose, AGEs, or LPS, have been recognized as major pathogenic events in the progression of renal failure in DN [25]. Accordingly, our study found 30 mmol/L glucose stimulation for 24 h induced decrease of Ca 2+ after a certain lag period; meanwhile, NLRP3 inflammasome signaling molecules and inflammatory cytokine IL-1β release from GMCs were induced by high glucose, suggesting that STRs could be involved in the activation of NLRP3 inflammasome under high-glucose stress.…”

Section: Genementioning

confidence: 99%

Sweet-Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation—Implications for Diabetic Nephropathy

Zhou¹,

Huang²,

Xu³

et al. 2018

Diabetes

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Previous studies demonstrated that ROS-NLRP3 inflammasome signaling activation was involved in the pathogenesis of diabetic nephropathy (DN). Recent research has shown that sweet taste receptors (STRs) are important sentinels of innate immunity. Whether high glucose primes ROS-NLRP3 inflammasome signaling via STRs is unclear. In this study, diabetic mouse model was induced by streptozotocin (STZ) in vivo; mouse glomerular mesangial cells (GMCs) and human proximal tubular cells were stimulated by high glucose (10, 20, and 30 mmol/L) in vitro; STR inhibitor lactisole was used as an intervention reagent to evaluate the role and mechanism of the STRs in the pathogenesis of DN. Our results showed that the expression of STRs and associated signaling components (Gα-gustducin, PLCβ2, and TRPM5) was obviously downregulated under the condition of diabetes in vivo and in vitro. Furthermore, lactisole significantly mitigated the production of intracellular ROS and reversed the high glucose-induced decrease of Ca 2+ and the activation of NLRP3 inflammasome signaling in vitro (p < 0 05). These combined results support the hypothesis that STRs could be involved in the activation of ROS-NLRP3 inflammasome signaling in the pathogenesis of DN, suggesting that STRs may act as new therapeutic targets of DN.

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“…There are numerous reports that showed beneficial effects of SCFAs in maintaining host immune function and intestinal barrier function; SCFAs serve as energy source for our body (in fact, our body has receptors for SCFAs) [8,9] , improve intestinal barrier function [10,11] , improve diabetes (through increasing production of incretin) [9,12] , inhibit allergic response (through improvement of regulatory T cell function) [13] , and scavenge oxygen radicals (by hydrogen produced in the process of SCFAs production) [14,15] . These functions may be more important when our body is exposed to a stressful condition such as that after a highly invasive abdominal surgery.…”

Section: Basic Knowledge Of Intestinal Microenvironmentmentioning

confidence: 99%

Effects of Synbiotics to Prevent Postoperative Infectious Complications in Highly Invasive Abdominal Surgery

et al. 2017

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Postoperative infectious complication (POIC) is one of the most common complications following highly invasive abdominal surgeries, such as hepatectomy, esophagectomy, and pancreatoduodenectomy. The surgical stress temporarily deteriorates the intestinal microenvironment, and the fecal concentrations of beneficial bacteria such as Bifidobacterium and Lactobacillus decrease following highly invasive abdominal surgery. In parallel with these changes, the concentrations of fecal short-chain fatty acids (SCFAs) such as acetic acid, propionic acid, and butyric acid also decrease after surgery. In contrast, the fecal concentration of lactic acid increases under this condition because of the deterioration of the metabolism from lactic acid to SCFAs by normal intestinal microflora. Decreased fecal concentration of SCFAs may lead to an impaired intestinal barrier function under stressful condition. Translocation of bacteria from the gut to lymphatic and bloodstream leads to bacteremia and subsequent POICs. The incidence of POICs in patients with unhealthy intestinal microflora before surgery may be more because their intestine is more susceptible to bacterial translocation induced by surgical stress. Therefore, improving the intestinal microenvironment and intestinal barrier function before surgery is crucial to prevent POICs following highly invasive abdominal surgeries. In this regard, the use preoperative synbiotics therapy may be one of the effective ways because it has been shown to improve intestinal microflora, increase fecal SCFAs, prevent bacterial translocation, and reduce the incidence of POICs in several randomized controlled trial in patients undergoing highly invasive abdominal surgeries.

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Short-Chain Fatty Acids Inhibit Oxidative Stress and Inflammation in Mesangial Cells Induced by High Glucose and Lipopolysaccharide

Cited by 144 publications

References 21 publications

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

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

Sweet-Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation—Implications for Diabetic Nephropathy

Effects of Synbiotics to Prevent Postoperative Infectious Complications in Highly Invasive Abdominal Surgery

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