Effects of resistance physical exercise in neutrophils and lymphocytes from knockout mice for TNF-<font face=\"Symbol\">a receptor 1.

O objetivo desse estudo foi verificar os efeitos do treinamento resistido agudo (única sessão - TA) e de 5 semanas de exercício crônico (TC) sobre a apoptose de neutrófilos e linfócitos de camundongos controle e nocaute para TNFR1. Determinamos: viabilidade, externalização de fosfatidilserina, fragmentação do DNA e potencial de membrana mitocondrial. O ensaio do conteúdo de lipídeos neutros foi realizado em neutrófilos e a proliferação em linfócitos. TA e TC não alteraram os parâmetros avaliados nos neutrófilos. Não houve alteração nos linfócitos dos camundongos que realizaram TA. Porém, o TC aumentou a porcentagem de linfócitos com externalização de fosfatidilserina e diminuiu a proliferação dessa células nos camundongos selvagens. O exercício crônico aumentou a proporção de linfócitos em apoptose e diminuiu a proliferação nos camundongos nocaute para TNFR1. Concluímos então que a via do TNFR1 está envolvida neste processo.The aim of this study was to investigate the acute or chronic effects of resistance exercise training on apoptosis of neutrophils and lymphocytes from knockout mice for TNF-a receptor 1 and control mice. The following parameters were determined viability, externalization of phosphatidylserine on the plasma membrane, DNA fragmentation and mitochondrial membrane potential. The measurement of the content of neutral lipids was performed in neutrophils only and the proliferation assay in lymphocytes. The acute and chronic exercise did not alter the parameters evaluated in neutrophils. Acute exercised also did not affect lymphocyte function. However, chronic resistance exercise increased the percentage of lymphocytes with phosphatidylserine externalization and decreased lymphocyte proliferation capacity of wild type mice. Chronic exercise raised the proportion of lymphocytes in apoptosis and decreased lymphocyte proliferation in TNFR1 knockout mice. We concluded that the effect of chronic exercise on lymphocyte death involves the TNFR1 pathway

Fatty Acids As Modulators Of Neutrophil Recruitment, Function And Survival.

Neutrophils are well-known to act in the destruction of invading microorganisms. They have also been implicated in the activation of other immune cells including B- and T-lymphocytes and in the resolution of inflammation and tissue regeneration. Neutrophils are produced in the bone marrow and released into the circulation from where they migrate to tissues to perform their effector functions. Neutrophils are in constant contact with fatty acids that can modulate their function, activation and fate (survival or cell death) through different mechanisms. In this review, the effects of fatty acids pertaining to five classes, namely, long-chain saturated fatty acids (LCSFAs), short-chain fatty acids (SCFAs), and omega-3 (n-3), omega-6 (n-6) and omega-9 (n-9) unsaturated fatty acids, on neutrophils and the relevance of these effects for disease development are discussed

Tributyrin Attenuates Metabolic and Inflammatory Changes Associated with Obesity through a GPR109A-Dependent Mechanism

Obesity is linked with altered microbial short-chain fatty acids (SCFAs), which are a signature of gut dysbiosis and inflammation. In the present study, we investigated whether tributyrin, a prodrug of the SCFA butyrate, could improve metabolic and inflammatory profiles in diet-induced obese mice. Mice fed a high-fat diet for eight weeks were treated with tributyrin or placebo for another six weeks. We show that obese mice treated with tributyrin had lower body weight gain and an improved insulin responsiveness and glucose metabolism, partly via reduced hepatic triglycerides content. Additionally, tributyrin induced an anti-inflammatory state in the adipose tissue by reduction of Il-1&beta; and Tnf-a and increased Il-10, Tregs cells and M2-macrophages. Moreover, improvement in glucose metabolism and reduction of fat inflammatory states associated with tributyrin treatment were dependent on GPR109A activation. Our results indicate that exogenous targeting of SCFA butyrate attenuates metabolic and inflammatory dysfunction, highlighting a potentially novel approach to tackle obesity

Effect of the marathon race on muscle damage markers and CRP.

<p>The plasma was separated before, immediately after, 24 h after, and 72 h after the marathon race. The plasma activities of LDH (A), CK (C), CK-MB (D), and plasma levels of CRP (B) were determined. The values presented are the mean ± SEM of 23 runners.^a p<0.001 vs before the marathon race, ^b p<0.0001 vs immediately after the marathon race, and ^c p<0.01 vs 24 h after the marathon race.</p

Effect of the marathon race on neutrophil surface molecules and DNA fragmentation.

<p>Neutrophils were separated after blood collection before, immediately after, 24 h after, and 72 h after the marathon race. Expression of ICAM-1 (A), TNFR1 receptor (B), L-selectin (C), and Fas receptor (D), and % of cells with DNA fragmentation (D) were determined. The fluorescence was determined by flow cytometry (BD Accuri cytometer). The values presented are the mean ± SEM of 21 runners. ^a p<0.05 vs before the marathon race, ^b p<0.05 vs immediately after the marathon race, and ^cp<0.05 vs 24 h after the marathon race.</p

Model on the temporal dynamics of the cytokine’s responses to the marathon race.

<p>Model on the temporal dynamics of the cytokine’s responses to the marathon race.</p

Effect of the marathon race on hematological parameters.

<p>Total leukocyte number (A), neutrophil number (B), hematocrit (C), and hemoglobin (D) were determined before, immediately after, 24 h, and 72 h after the marathon race. The values presented are the mean ± SEM of 23 runners.^ap<0.05 vs before the marathon race, ^bp<0.05 vs immediately after the marathon race, and ^cp<0.05 vs 24 h after the marathon race.</p

Effect of the marathon race on plasma cytokines.

<p>Plasma concentrations of IL-6 (A), IL-8 (B) IL-10 (C), IL-12 (D), and TNF-alpha (E) were determined using cytometric bead array. The values presented are the mean ± SEM of 23 runners.^ap<0.05 vs before the marathon race, ^bp<0.05vs immediately after the marathon race, and ^c p<0.05 vs 24 h after the marathon race.</p