Effects of acute exercise on monocyte subpopulations in metabolic syndrome patients

Wonner, Ralph; Wallner, Stefan; Orsó, Evelyn; Schmitz, Gerd

doi:10.1002/cyto.b.21387

Cited by 7 publications

(7 citation statements)

References 56 publications

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“…38 Although the percentage of monocytes in the present study are unknown, and therefore the authors cannot verify whether the percentage of monocyte subsets are different among obese and normal-weight individuals at rest or in response to acute aerobic exercise, a recent study has demonstrated that obesity does not influence the distribution of monocyte subsets immediately following acute exercise. 32 Therefore, further studies are necessary to examine the phenotypic changes of monocytes in response to acute aerobic exercise as a mechanism to explain the suppressed production of PTX3 and IL-10 that was observed in both obese and normal-weight groups in the present study.…”

Section: Discussionmentioning

confidence: 79%

Exercise reduced pentraxin 3 levels produced by endotoxin-stimulated human peripheral blood mononuclear cells in obese individuals

Slusher

Shibata

Whitehurst

et al. 2017

Exp Biol Med (Maywood)

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Impact statementOur laboratory has previously demonstrated that obese individuals present with lower plasma concentrations of the antiinflammatory protein pentraxin 3 (PTX3), whereas acute aerobic exercise increases plasma PTX3 levels similarly compared to normal-weight individuals. As a follow-up, the present study demonstrates that PBMCs isolated from obese and normalweight individuals produce comparable amounts of PTX3 ex vivo in response to lipopolysaccharide (LPS). Furthermore, given that acute aerobic exercise reduced the ex vivo production of PTX3 in both groups, our results clearly indicate that plasma PTX3 levels are relatively independent of those produced by PBMCs ex vivo. In addition, our findings suggest that the mechanisms associated with PTX3-mediated production of the anti-inflammatory cytokine interleukin 10 may be impaired in obese individuals, and thus provides a key finding necessary for the elucidation of PTX3's role in the mediation of anti-inflammatory profiles and the subsequent amelioration of inflammatory disease during obesity. AbstractThe purpose of this study was to determine whether obesity would reduce the capacity of peripheral blood mononuclear cells (PBMCs) to produce the anti-inflammatory protein pentraxin 3 (PTX3) in response to ex vivo stimulation with lipopolysaccharide (LPS), and if acute aerobic exercise would enhance this PTX3 production capacity. In addition, the inter-relationships of LPS-induced PTX3 with the inflammatory cytokines (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha) were examined. Twenty-one healthy subjects (10 obese and 11 normal-weight) performed an acute bout of aerobic exercise at 75% VO 2max . The capacity of PBMCs to produce PTX3 ex vivo following LPS stimulation was the same in obese and normal-weight subjects at rest, and decreased equally in both subject groups following acute aerobic exercise. This is in contrast to plasma PTX3, which is lower in obese subjects at rest and increased equally in both obese and normal-weight subjects following exercise. In addition, ex vivo PTX3 production was positively associated with IL-6 and IL-10 in response to acute aerobic exercise (r ¼ 0.686, P ¼ 0.020; r ¼ 0.744, P ¼ 0.009, respectively) in normal-weight, but not in obese individuals (r ¼ 0.429, P ¼ 0.249; r ¼ 0.453, P ¼ 0.189, respectively). These findings indicate that concentrations of PTX3 observed in plasma are relatively independent of those produced by PBMCs ex vivo and the mechanisms associated with PTX3-mediated anti-inflammatory signaling may differ during obesity.

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Section: Discussionmentioning

confidence: 79%

Exercise reduced pentraxin 3 levels produced by endotoxin-stimulated human peripheral blood mononuclear cells in obese individuals

Slusher

Shibata

Whitehurst

et al. 2017

Exp Biol Med (Maywood)

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“…Some studies have demonstrated that an acute bout of strenuous exercise induced a significant increase in nonclassical monocyte proportion in both healthy [ 58 – 60 ] and obese individuals [ 61 , 62 ]. It was postulated that the greater catecholaminergic response, the degree of muscle damage and oxidative stress response mediates the proinflammatory monocyte mobilization.…”

Section: Discussionmentioning

confidence: 99%

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

Dorneles¹,

Boeira

Schipper

et al. 2017

Oxidative Medicine and Cellular Longevity

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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.

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“…It is possible that methodological differences (e.g. gating strategy, anticoagulant, monocyte selection, staining techniques) or even unanticipated human pre-existing conditions 56,57 could account for some of these differences. The relative frequency of CD16− and CD16+ monocytes before and after plasma-free homeostatic extravasation confirmed that both adult and newborn CD16+ monocytes are preferential extravasators in our vascular model.…”

Section: Discussionmentioning

confidence: 99%

Neonatal monocytes demonstrate impaired homeostatic extravasation into a microphysiological human vascular model

Sánchez-Schmitz

Morrocchi

Cooney

et al. 2020

Sci Rep

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Infections are most frequent at the extremes of life, especially among newborns, reflecting age-specific differences in immunity. Monocytes maintain tissue-homeostasis and defence-readiness by escaping circulation in the absence of inflammation to become tissue-resident antigen presenting cells in vivo. Despite equivalent circulating levels, neonates demonstrate lower presence of monocytes inside peripheral tissues as compared to adults. To study the ability of monocytes to undergo autonomous transendothelial extravasation under biologically accurate circumstances we engineered a three-dimensional human vascular-interstitial model including collagen, fibronectin, primary endothelial cells and autologous untreated plasma. This microphysiological tissue construct enabled age-specific autonomous extravasation of monocytes through a confluent human endothelium in the absence of exogenous chemokines and activation. Both CD16− and CD16+ newborn monocytes demonstrated lower adherence and extravasation as compared to adults. In contrast, pre-activated tissue constructs were colonized by newborn monocytes at the same frequency than adult monocytes, suggesting that neonatal monocytes are capable of colonizing inflamed tissues. The presence of autologous plasma neither improved newborn homeostatic extravasation nor shaped age-specific differences in endothelial cytokines that could account for this impairment. Newborn monocytes demonstrated significantly lower surface expression of CD31 and CD11b, and mechanistic experiments using blocking antibodies confirmed a functional role for CD31 and CD54 in neonatal homeostatic extravasation. Our data suggests that newborn monocytes are intrinsically impaired in extravasation through quiescent endothelia, a phenomenon that could contribute to the divergent immune responsiveness to vaccines and susceptibility to infection observed during early life.

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Effects of acute exercise on monocyte subpopulations in metabolic syndrome patients

Cited by 7 publications

References 56 publications

Exercise reduced pentraxin 3 levels produced by endotoxin-stimulated human peripheral blood mononuclear cells in obese individuals

Exercise reduced pentraxin 3 levels produced by endotoxin-stimulated human peripheral blood mononuclear cells in obese individuals

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

Neonatal monocytes demonstrate impaired homeostatic extravasation into a microphysiological human vascular model

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