Short-chain fatty acids produced by anaerobic bacteria alter the physiological responses of human neutrophils to chemotactic peptide

Eftimiadi, C.; Buzzi, E; Tonetti, Michela; Buffa, Piero; Buffa, D; Steenbergen, M.T.J. van; Graaff, J. de; Botta, Giuseppe

doi:10.1016/s0163-4453(87)90808-5

Cited by 84 publications

(51 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1,40,41 The effect of butyrate on PMA-and fMLP-induced ROS production by neutrophils was previously reported by others. 14,17,19,21 The inhibition of ROS production by butyrate reported herein was not due to modulation of expression of NADPH oxidase components, but it was associated to reduced phosphorylation of the regulatory subunit p47phox. The inhibitory effect of butyrate on 42 GPR43 can be activated by SCFAs and is highly expressed in neutrophils and monocytes being coupled to Gi/o and Gq proteins.…”

Section: Discussionmentioning

confidence: 66%

Effects of short chain fatty acids on effector mechanisms of neutrophils

Vinolo

Hatanaka

Lambertucci

et al. 2008

Cell Biochemistry & Function

105

View full text Add to dashboard Cite

Short chain fatty acids (SCFAs) are metabolic by products of anaerobic bacteria fermentation. These fatty acids, despite being an important fuel for colonocytes, are also modulators of leukocyte function. The aim of this study was to evaluate the effects of SCFAs (acetate, propionate, and butyrate) on function of neutrophils, and the possible mechanisms involved. Neutrophils obtained from rats by intraperitoneal lavage 4 h after injection of oyster glycogen solution (1%) were treated with non toxic concentrations of the fatty acids. After that, the following measurements were performed: phagocytosis and destruction of Candida albicans, production of ROS (O(2)(*-), H(2)O(2), and HOCl) and degranulation. Gene expression (p47(phox) and p22(phox)) and protein phosphorylation (p47(phox)) were analyzed by real time reverse transcriptase chain reaction (RT-PCR) and Western blotting, respectively. Butyrate inhibited phagocytosis and killing of C. albicans. This SCFA also had an inhibitory effect on production of O(2)(*-), H(2)O(2), and HOCl by neutrophils stimulated with PMA or fMLP. This effect of butyrate was not caused by modulation of expression of NADPH oxidase subunits (p47(phox) and p22(phox)) but it was in part due to reduced levels of p47(phox) phosphorylation and an increase in the concentration of cyclic AMP. Acetate increased the production of O(2)(*-) and H(2)O(2) in the absence of stimuli but had no effect on phagocytosis and killing of C. albicans. Propionate had no effect on the parameters studied. These results suggest that butyrate can modulate neutrophil function and thus could be important in inflammatory neutrophil-associated diseases.

show abstract

Section: Discussionmentioning

confidence: 66%

Effects of short chain fatty acids on effector mechanisms of neutrophils

Vinolo

Hatanaka

Lambertucci

et al. 2008

Cell Biochemistry & Function

105

View full text Add to dashboard Cite

show abstract

“…Previous researches showed that acetate obviously inhibited the activation of neutrophils which can produce amount of ROS. [39][40][41] Therefore, anti-oxidation function of acetate may be attributable to the inhibition of neutrophils.…”

Section: Fig 2 Histopathological Evaluation Of the Effects Of Acetamentioning

confidence: 99%

Short Chain Fatty Acid Acetate Protects against Ethanol-Induced Acute Gastric Mucosal Lesion in Mice

Liu

Wang

Shi

et al. 2017

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Short chain fatty acids acetate and propionate have been demonstrated protective function in the intestinal mucosa. However, their impact on gastric mucosa has not yet been elucidated. The current study aimed to investigate the potential protective effects of acetate and propionate against ethanol-induced gastric mucosal lesion and the underlying mechanism in mice. ICR mice were orally treated with acetate and propionate, respectively, 30 min prior to the establishment of gastric mucosal injury model by challenge with absolute ethanol. The gastric samples were collected for the detection of oxidative, inflammatory and apoptotic related parameters. Acetate, but not propionate, attenuated the severity of gastric mucosal damage as evidenced by the gross changes of gastric mucosa, pathological aberrations. Acetate alleviated oxidative stress as shown by the increase in glutathione (GSH) content and superoxide dismutase (SOD) activities, and the decrease of malondialdehyde (MDA) level. The elevated concentrations of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6, and the activation of nuclear factor-kappaB (NF-κB) p65 by ethanol stimulation was also reduced by acetate. Moreover, the anti-inflammatory factors, IL-4, LXA4 and IL-10, were up-regulated in acetate treated group. With respect to gastric mucosal apoptosis, acetate suppressed caspase-3 activity and BAX expression in favor of cell survival. These favorable actions were maybe associated with up-regulation of the gastric MUC5AC, the key defense factor of gastric mucosal system. These findings accentuate the gastroprotective actions of acetate in ethanol-induced gastric injury which were mediated via concerted multiprolonged actions, including suppression of gastric oxidation, inflammation and apoptosis and promotion of MUC5AC expression.

show abstract

“…[8][9][10] Short-chain FFAs have been described as displaying activities on leukocyte populations, particularly PMN cells. [15][16][17] Stimulation of PMN cells by propionate or acetate results in a transient increase in intracellular calcium.…”

mentioning

confidence: 99%