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Acute exercise-induced response of monocyte subtypes in chronic heart and renal failure.

Van Craenenbroeck AH, Van Ackeren K, Hoymans VY, Roeykens J, Verpooten GA, Vrints CJ, Couttenye MM, Van Craenenbroeck EM - Mediators Inflamm. (2014)

Bottom Line: Following acute exercise, %Mon2 and %Mon3 increased significantly at the expense of a decrease in %Mon1 in HS and in CKD.This response was significantly attenuated in CHF (P < 0.05).In HS only, MCP-1 levels increased following exercise; IL-6 levels were unchanged.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, 2650 Antwerp, Belgium ; Department of Nephrology, Antwerp University Hospital, 2650 Antwerp, Belgium ; Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, 2650 Antwerp, Belgium.

ABSTRACT

Purpose: Monocytes (Mon1-2-3) play a substantial role in low-grade inflammation associated with high cardiovascular morbidity and mortality of patients with chronic kidney disease (CKD) and chronic heart failure (CHF). The effect of an acute exercise bout on monocyte subsets in the setting of systemic inflammation is currently unknown. This study aims (1) to evaluate baseline distribution of monocyte subsets in CHF and CKD versus healthy subjects (HS) and (2) to evaluate the effect of an acute exercise bout. Exercise-induced IL-6 and MCP-1 release are related to the Mon1-2-3 response.

Methods: Twenty CHF patients, 20 CKD patients, and 15 HS were included. Before and after a maximal cardiopulmonary exercise test, monocyte subsets were quantified by flow cytometry: CD14(++)CD16(-)CCR2(+) (Mon1), CD14(++)CD16(+)CCR2(+) (Mon2), and CD14(+)CD16(++)CCR2(-) (Mon3). Serum levels of IL-6 and MCP-1 were determined by ELISA.

Results: Baseline distribution of Mon1-2-3 was comparable between the 3 groups. Following acute exercise, %Mon2 and %Mon3 increased significantly at the expense of a decrease in %Mon1 in HS and in CKD. This response was significantly attenuated in CHF (P < 0.05). In HS only, MCP-1 levels increased following exercise; IL-6 levels were unchanged. Circulatory power was a strong and independent predictor of the changes in Mon1 (β = -0.461, P < 0.001) and Mon3 (β = 0.449, P < 0.001); and baseline LVEF of the change in Mon2 (β = 0.441, P < 0.001).

Conclusion: The response of monocytes to acute exercise is characterized by an increase in proangiogenic and proinflammatory Mon2 and Mon3 at the expense of phagocytic Mon1. This exercise-induced monocyte subset response is mainly driven by hemodynamic changes and not by preexistent low-grade inflammation.

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Magnitude of the exercise-induced effect on monocyte count, monocyte subsets, and serum MCP-1 and IL-6 levels. (a) Following peak exercise, absolute monocyte count increased significantly in all groups. (b–d) Within the total monocyte count, the percentage of Mon1 decreased in all three groups with a parallel increase in Mon2 and Mon3 (with exception of Mon2 in CHF). Between-group analysis revealed that the overall response of the monocyte subsets was comparable between HS and CKD but was significantly blunted for patients with CHF (P for interaction <0.05 for all subsets). (e) Following peak exercise, MCP-1 levels increased significantly in HS but remained unchanged in patients with CKD and CHF (P = 0.004 for interaction). (f) Increase in IL-6 levels were observed in all groups but failed to reach the level of significance (HS P = 0.08; CKD P = 0.644; CHF P = 0.063). Changes in monocyte subset are expressed as % change from baseline. ***P < 0.001, **P < 0.01, and *P < 0.05.
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fig2: Magnitude of the exercise-induced effect on monocyte count, monocyte subsets, and serum MCP-1 and IL-6 levels. (a) Following peak exercise, absolute monocyte count increased significantly in all groups. (b–d) Within the total monocyte count, the percentage of Mon1 decreased in all three groups with a parallel increase in Mon2 and Mon3 (with exception of Mon2 in CHF). Between-group analysis revealed that the overall response of the monocyte subsets was comparable between HS and CKD but was significantly blunted for patients with CHF (P for interaction <0.05 for all subsets). (e) Following peak exercise, MCP-1 levels increased significantly in HS but remained unchanged in patients with CKD and CHF (P = 0.004 for interaction). (f) Increase in IL-6 levels were observed in all groups but failed to reach the level of significance (HS P = 0.08; CKD P = 0.644; CHF P = 0.063). Changes in monocyte subset are expressed as % change from baseline. ***P < 0.001, **P < 0.01, and *P < 0.05.

Mentions: In all 3 groups, percentage of Mon1 decreased, whereas Mon2 and Mon3 increased after a single bout (with exception of Mon2 in CHF, Table 3). Figure 2 illustrates that the magnitude of this exercise-induced effect on monocyte subsets is different in the 3 groups. The overall exercise-induced response on monocyte subsets was comparable between HS and CKD but was blunted in patients with CHF (P for interaction <0.05 for all subsets). In CHF, the decrease in Mon1 was less prominent, the increase in Mon2 was nearly absent, and the increase in Mon3 again was less pronounced.


Acute exercise-induced response of monocyte subtypes in chronic heart and renal failure.

Van Craenenbroeck AH, Van Ackeren K, Hoymans VY, Roeykens J, Verpooten GA, Vrints CJ, Couttenye MM, Van Craenenbroeck EM - Mediators Inflamm. (2014)

Magnitude of the exercise-induced effect on monocyte count, monocyte subsets, and serum MCP-1 and IL-6 levels. (a) Following peak exercise, absolute monocyte count increased significantly in all groups. (b–d) Within the total monocyte count, the percentage of Mon1 decreased in all three groups with a parallel increase in Mon2 and Mon3 (with exception of Mon2 in CHF). Between-group analysis revealed that the overall response of the monocyte subsets was comparable between HS and CKD but was significantly blunted for patients with CHF (P for interaction <0.05 for all subsets). (e) Following peak exercise, MCP-1 levels increased significantly in HS but remained unchanged in patients with CKD and CHF (P = 0.004 for interaction). (f) Increase in IL-6 levels were observed in all groups but failed to reach the level of significance (HS P = 0.08; CKD P = 0.644; CHF P = 0.063). Changes in monocyte subset are expressed as % change from baseline. ***P < 0.001, **P < 0.01, and *P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig2: Magnitude of the exercise-induced effect on monocyte count, monocyte subsets, and serum MCP-1 and IL-6 levels. (a) Following peak exercise, absolute monocyte count increased significantly in all groups. (b–d) Within the total monocyte count, the percentage of Mon1 decreased in all three groups with a parallel increase in Mon2 and Mon3 (with exception of Mon2 in CHF). Between-group analysis revealed that the overall response of the monocyte subsets was comparable between HS and CKD but was significantly blunted for patients with CHF (P for interaction <0.05 for all subsets). (e) Following peak exercise, MCP-1 levels increased significantly in HS but remained unchanged in patients with CKD and CHF (P = 0.004 for interaction). (f) Increase in IL-6 levels were observed in all groups but failed to reach the level of significance (HS P = 0.08; CKD P = 0.644; CHF P = 0.063). Changes in monocyte subset are expressed as % change from baseline. ***P < 0.001, **P < 0.01, and *P < 0.05.
Mentions: In all 3 groups, percentage of Mon1 decreased, whereas Mon2 and Mon3 increased after a single bout (with exception of Mon2 in CHF, Table 3). Figure 2 illustrates that the magnitude of this exercise-induced effect on monocyte subsets is different in the 3 groups. The overall exercise-induced response on monocyte subsets was comparable between HS and CKD but was blunted in patients with CHF (P for interaction <0.05 for all subsets). In CHF, the decrease in Mon1 was less prominent, the increase in Mon2 was nearly absent, and the increase in Mon3 again was less pronounced.

Bottom Line: Following acute exercise, %Mon2 and %Mon3 increased significantly at the expense of a decrease in %Mon1 in HS and in CKD.This response was significantly attenuated in CHF (P < 0.05).In HS only, MCP-1 levels increased following exercise; IL-6 levels were unchanged.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, 2650 Antwerp, Belgium ; Department of Nephrology, Antwerp University Hospital, 2650 Antwerp, Belgium ; Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, 2650 Antwerp, Belgium.

ABSTRACT

Purpose: Monocytes (Mon1-2-3) play a substantial role in low-grade inflammation associated with high cardiovascular morbidity and mortality of patients with chronic kidney disease (CKD) and chronic heart failure (CHF). The effect of an acute exercise bout on monocyte subsets in the setting of systemic inflammation is currently unknown. This study aims (1) to evaluate baseline distribution of monocyte subsets in CHF and CKD versus healthy subjects (HS) and (2) to evaluate the effect of an acute exercise bout. Exercise-induced IL-6 and MCP-1 release are related to the Mon1-2-3 response.

Methods: Twenty CHF patients, 20 CKD patients, and 15 HS were included. Before and after a maximal cardiopulmonary exercise test, monocyte subsets were quantified by flow cytometry: CD14(++)CD16(-)CCR2(+) (Mon1), CD14(++)CD16(+)CCR2(+) (Mon2), and CD14(+)CD16(++)CCR2(-) (Mon3). Serum levels of IL-6 and MCP-1 were determined by ELISA.

Results: Baseline distribution of Mon1-2-3 was comparable between the 3 groups. Following acute exercise, %Mon2 and %Mon3 increased significantly at the expense of a decrease in %Mon1 in HS and in CKD. This response was significantly attenuated in CHF (P < 0.05). In HS only, MCP-1 levels increased following exercise; IL-6 levels were unchanged. Circulatory power was a strong and independent predictor of the changes in Mon1 (β = -0.461, P < 0.001) and Mon3 (β = 0.449, P < 0.001); and baseline LVEF of the change in Mon2 (β = 0.441, P < 0.001).

Conclusion: The response of monocytes to acute exercise is characterized by an increase in proangiogenic and proinflammatory Mon2 and Mon3 at the expense of phagocytic Mon1. This exercise-induced monocyte subset response is mainly driven by hemodynamic changes and not by preexistent low-grade inflammation.

Show MeSH
Related in: MedlinePlus