Butyrate enhances the production of nitric oxide in mouse vascular endothelial cells in response to gamma interferon

Morikawa, Akiko; Sugiyama, Tsuyoshi; Koide, Naoki; Mori, Ikue; Mu, Mya Mya; Yoshida, Tomoaki; Hassan, Ferdaus; Islam, Shamima; Yokochi, Takashi

doi:10.1179/096805104225003852

Cited by 12 publications

(7 citation statements)

References 18 publications

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“…The RNA-Seq and IHC analyses did not suggest any increases in pro-inflammatory cytokines (e.g., TNF, IL-1, and VEGF) or altered cellular infiltrates that might be associated with increased edema. Instead, we speculate that butyrate is promoting edema (at least in part) by acting on endothelial cells (24, 168). CHIKV infects endothelial cells in vivo (37, 169) and edema is a well-known symptom of CHIKV infection (47, 82).…”

Section: Discussionmentioning

confidence: 87%

Exacerbation of Chikungunya Virus Rheumatic Immunopathology by a High Fiber Diet and Butyrate

et al. 2019

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Chikungunya virus (CHIKV) is a mosquito transmitted alphavirus associated with a robust systemic infection and an acute inflammatory rheumatic disease. A high fiber diet has been widely promoted for its ability to ameliorate inflammatory diseases. Fiber is fermented in the gut into short chain fatty acids such as acetate, propionate, and butyrate, which enter the circulation providing systemic anti-inflammatory activities. Herein we show that mice fed a high fiber diet show a clear exacerbation of CHIKV arthropathy, with increased edema and neutrophil infiltrates. RNA-Seq analyses illustrated that a high fiber diet, in this setting, promoted a range of pro-neutrophil responses including Th17/IL-17. Gene Set Enrichment Analyses demonstrated significant similarities with mouse models of inflammatory psoriasis and significant depression of macrophage resolution phase signatures in the CHIKV arthritic lesions from mice fed a high fiber diet. Supplementation of the drinking water with butyrate also increased edema after CHIKV infection. However, the mechanisms involved were different, with modulation of AP-1 and NF-κB responses identified, potentially implicating deoptimization of endothelial barrier repair. Thus, neither fiber nor short chain fatty acids provided benefits in this acute infectious disease setting, which is characterized by widespread viral cytopathic effects and a need for tissue repair.

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Section: Discussionmentioning

confidence: 87%

Exacerbation of Chikungunya Virus Rheumatic Immunopathology by a High Fiber Diet and Butyrate

et al. 2019

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“…Butyrate is an inhibitor of histone deacetylase (HDAC) which also interferes with NF-B activation (Licciardi et al, 2011). However, in certain cells such as murine vascular endothelial cell END-D and N9 microglial cells it was shown to augment NO production (Glozak et al, 2005;Huuskonen et al, 2004;Morikawa et al, 2004). Phorbol myristate acetate is an activator of protein kinase C which stimulates respiratory burst activities in macrophages (Green and Phillips, 1994;Rath et al, 2003).…”

Section: Discussionmentioning

confidence: 98%

Effect of butyrate on immune response of a chicken macrophage cell line

Zhou

Packialakshmi

Makkar

et al. 2014

Veterinary Immunology and Immunopathology

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“…Here we report that butyrate supplementation increases plasma levels of LBP. However, this effect may be muted by the addition of butyrate, as several groups have reported reductions in the downstream effects of LPS-mediated induction of the immune system (Chakravortty et al, 2000;Huuskonen et al, 2004;Morikawa et al, 2004;Ni et al, 2010) under similar conditions. In addition, SAA, also an acute phase protein, was unaffected by the addition of butyrate.…”

Section: Physiological Parametersmentioning

confidence: 97%

Butyrate-Mediated Genomic Changes Involved in Non-Specific Host Defenses, Matrix Remodeling and the Immune Response in the Rumen Epithelium of Cows Afflicted With Subacute Ruminal Acidosis

Dionissopoulos

Laarman

AlZahal

et al. 2013

American Journal of Animal and Veterinary Sciences

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Subacute Ruminal Acidosis (SARA) is a disorder in cattle which can lead to chronic inflammation in the rumen epithelium, known as rumenitis. Butyrate has been shown to attenuate some of the detrimental effects of inflammatory gastroenteral disorders but the molecular mechanisms mediated by butyrate have not been defined. The objective of this study was to define the inflammatory-related genomic changes responsible for the beneficial effects of butyrate. Experimentally, 16 fistulated dairy cows at mid-lactation were fed a SARA-inducing (45% non-fiber carbohydrate) diet beginning 2 days before the beginning of treatment and continuing throughout the experiment. Cows were then evenly divided into treatment groups where a carrier with (n = 8) or without (n = 8) supplemental butyrate (2.5% initial DM intake) was deposited into the rumen daily for 7 days. The minimum rumen pH was higher in cows with supplemental butyrate (4.96±0.09 to 5.20±0.05, p = 0.040), but mean pH, maximum pH and the duration for which rumen pH was below 5.6 was unaffected. Free plasma Lipopolysaccharide (LPS) concentration was unaffected by treatment as was the concentration of Serum Amyloid A (SAA), although the LPS Binding Protein (LBP) concentration was increased by the addition of butyrate to the rumen (6.91±0.29 to 7.93±0.29 µg mL −1 , p = 0.024). Of the rumen Short Chain Fatty Acids (SCFA) tested, only butyrate showed a pronounced treatment effect, rising from 8.60±0.94 to 21.60±0.94 mM (p≤0.0001). Plasma Beta-Hydroxybutyrate (BHBA) concentration also increased (799.50±265.24 to 3261.63±265.24 µM, p≤0.001). Butyrate infusion did not affect milk parameters (total fat, lactose, total protein and LOS); however, when related to dry matter intake, milk production efficiency was increased (p = 0.035). Microarray and qRT-PCR analyses of rumen papillae biopsies collected on day 7 found that butyrate administration affected (p≤0.05) the expression of genes involved in Non-Specific Host Defense (NSHD), Remodeling or adaptation (RM) and Immune Response (IR). Of the 49 genes tested by qRT-PCR, 9 (LCN2, MMP1, MUC16, GPX2, CSTA, FUT1, SERPINE2, BCAM, RAC3) were upregulated, 20 (MTOR, AKIRIN2, NFKBIZ, NFKB2, ACVR2A, LAMB1, FRS2, PPARD, LBP, NEDD4L, SGK1, DEDD2, MAP3K8, PARD6B, PLIN2, ADA, HPGD, FMO5, BMP6, TCHH) were downregulated and 20 were unchanged due to butyrate administration in the proximal gastrointestinal tract. AJAVSThese results demonstrate the potential protective effect and molecular mechanisms involved in a novel butyrate treatment for inflammatory gastrointestinal conditions.

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Butyrate enhances the production of nitric oxide in mouse vascular endothelial cells in response to gamma interferon

Cited by 12 publications

References 18 publications

Exacerbation of Chikungunya Virus Rheumatic Immunopathology by a High Fiber Diet and Butyrate

Exacerbation of Chikungunya Virus Rheumatic Immunopathology by a High Fiber Diet and Butyrate

Effect of butyrate on immune response of a chicken macrophage cell line

Butyrate-Mediated Genomic Changes Involved in Non-Specific Host Defenses, Matrix Remodeling and the Immune Response in the Rumen Epithelium of Cows Afflicted With Subacute Ruminal Acidosis

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