Soluble interleukin-1 receptor type 2 plasma levels in Parkinson’s disease: relationship with cardiac autonomic profile before and after peripheral mechanical somatosensory stimulation
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Autor
Shiffer, Dana
Zamunér, Antonio
Minonzio, Maura
Bulgheroni, Mara
Porta, Alberto
Leone, Roberto
Bottazzi, Barbara
Garlanda, Cecilia
Colotta, Francesco
Barbic, Franca
Mantovani, Alberto
Furlan, Raffaello
Fecha
2023Resumen
Introduction: Systemic inflammation promotes neurodegeneration in Parkinson’s disease (PD). Interleukin-1 receptor type 2 (sIL-1R2) plasma levels increase during inflammation. Data on sIL-1R2 in PD patients and its relationship with PD cardiac autonomic profile are limited, given the possible anti-inflammatory effect of vagal activation. Previously, automated mechanical peripheral somatosensory stimulation (AMPSS) enhanced cardiac vagal modulation. Objectives were to 1) evaluate sIL-1R2 plasma concentrations in PD patients and healthy controls and 2) investigate the correlations between sIL-1R2 and cardiac autonomic indices obtained by spectrum analysis of heart rate variability before and after AMPSS.
Methods: sIL-1R2 plasma levels were assessed in 48 PD patients and 50 healthy controls. Electrocardiogram and beat-by-beat arterial pressure were recorded at baseline and after 5 AMPSS sessions in 16 PD patients.
Results: PD patients had higher sIL-1R2 levels than controls. In the PD subgroup, an inverse correlation between sIL-1R2 and HFnu was found. There was a negative correlation between changes induced by AMPSS on HFnu and sIL-1R2.
Discussion: Higher sIL-1R2 levels in PD patients reflect the inflammatory dysregulation associated with the disease. In PD patients, higher sIL-1R2 was associated with reduced cardiovagal tone. Increased cardiovagal modulation following AMPSS was associated with lower sIL-1R2 levels in Parkinson’s disease patients, suggesting inflammatory state improvement.
Fuente
Frontiers in Physiology, 14, 1168652Link de Acceso
Click aquí para ver el documentoIdentificador DOI
doi.org/10.3389/fphys.2023.1168652Colecciones
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