Acute Strenuous Exercise Induces an Imbalance on Histone H4 Acetylation/Histone Deacetylase 2 and Increases the Proinflammatory Profile of PBMC of Obese Individuals

Author:

Dorneles Gilson P.1ORCID,Boeira Maria Carolina R.2,Schipper Lucas L.2,Silva Ivy R. V.2,Elsner Viviane R.2,Dal Lago Pedro3,Peres Alessandra123ORCID,Romão Pedro R. T.1ORCID

Affiliation:

1. Graduate Program in Health Sciences, Laboratory of Cellular and Molecular Immunology, Federal University of Health Sciences of Porto Alegre, 90050-170 Porto Alegre, RS, Brazil

2. Research Center, Graduate Program in Bioscience and Rehabilitation, Methodist University Center IPA, 90420-060 Porto Alegre, RS, Brazil

3. Graduate Program in Rehabilitation Sciences, Federal University of Health Sciences of Porto Alegre, 90050-170 Porto Alegre, RS, Brazil

Abstract

This study evaluated the response of global histone H4 acetylation (H4ac), histone deacetylase 2 (HDAC2) activity, as well as the production of proinflammatory cytokines and monocyte phenotypes of lean and obese males after exercise. Ten lean and ten obese sedentary men were submitted to one session of strenuous exercise, and peripheral blood mononuclear cells (PBMC) were stimulated in vitro with lipopolysaccharide (LPS). Global H4ac levels, HDAC2 activity in PBMC, and IL-6, IL-8, and TNF-α production were analyzed. Monocyte phenotype was determined in accordance with the expression of CD14 and CD16. At rest, obese individuals presented higher frequency of proinflammatory CD14+CD16+ monocytes. LPS induced a significant augment in global H4ac and in the production of IL-6, IL-8, and TNF-α mainly in obese individuals. After exercise, the increased production of IL-8 and TNF-α and peripheral frequency of CD14+CD16+ were observed in both groups. In addition, exercise also induced a significant hyperacetylation of histone H4 and decreased HDAC2 activity in both nonstimulated and LPS-stimulated PBMC of obese individuals. Our data indicate that the obesity impacts on H4ac levels and that strenuous exercise leads to an enhanced chronic low-grade inflammation profile in obesity via an imbalance on H4ac/HDAC2.

Funder

Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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