BACKGROUND: The aim of our study was to determine whether intermittent hemodiafiltration (HDF) leads to an alteration in monocyte antiviral activity as well as in the in vitro release of cytokines such as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-alpha) and interferon-alpha (IFN-alpha) by the same cells. METHODS: We enrolled 25 patients undergoing HDF for 3.5-4 hours 3 times a week (12 men, 13 women; mean age 58 +/- 6.7 years) and 25 healthy donors (ND) (12 men, 13 women; mean age 57 +/- 8 years). Monocytes from peripheral blood mononuclear cells were isolated with a Monocyte Isolation Kit II. Monocytic cells were infected with herpes simplex virus type 2 (HSV-2). Cytokines were assayed in supernatants. RESULTS: The in vitro antiviral activity of monocytes from HDF patients was significantly impaired with respect to ND. Furthermore, monocytes from post-HDF patients were more prone to viral infection. Lipopolysaccharide (LPS) stimulation induced significant viral inhibition only in monocytes from NDs (p<0.05). The cytokine pattern (TNF-alpha, IFN-alpha and IL-12) in monocytes stimulated with LPS was markedly inhibited in HDF patients compared with ND (p<0.05). A basal production of TNF-alpha was found in monocytes from pre-HDF and post-HDF patients. No IFN-alpha production was found in LPS-stimulated and HSV-2-infected monocytes from pre-HDF and post-HDF patients. IL-12 production appeared significantly decreased after HDF in all experimental conditions (p<0.05). CONCLUSIONS: The significant increase of viral replication in monocytes from HDF patients compared with healthy donors could be related to a significant reduction of cytokine production. Moreover, the dialytic session influenced the intrinsic antiviral activity of monocytes, favoring viral replication.
BACKGROUND: The aim of our study was to determine whether intermittent hemodiafiltration (HDF) leads to an alteration in monocyte antiviral activity as well as in the in vitro release of cytokines such as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-alpha) and interferon-alpha (IFN-alpha) by the same cells. METHODS: We enrolled 25 patients undergoing HDF for 3.5-4 hours 3 times a week (12 men, 13 women; mean age 58 +/- 6.7 years) and 25 healthy donors (ND) (12 men, 13 women; mean age 57 +/- 8 years). Monocytes from peripheral blood mononuclear cells were isolated with a Monocyte Isolation Kit II. Monocytic cells were infected with herpes simplex virus type 2 (HSV-2). Cytokines were assayed in supernatants. RESULTS: The in vitro antiviral activity of monocytes from HDF patients was significantly impaired with respect to ND. Furthermore, monocytes from post-HDF patients were more prone to viral infection. Lipopolysaccharide (LPS) stimulation induced significant viral inhibition only in monocytes from NDs (p<0.05). The cytokine pattern (TNF-alpha, IFN-alpha and IL-12) in monocytes stimulated with LPS was markedly inhibited in HDF patients compared with ND (p<0.05). A basal production of TNF-alpha was found in monocytes from pre-HDF and post-HDF patients. No IFN-alpha production was found in LPS-stimulated and HSV-2-infected monocytes from pre-HDF and post-HDF patients. IL-12 production appeared significantly decreased after HDF in all experimental conditions (p<0.05). CONCLUSIONS: The significant increase of viral replication in monocytes from HDF patients compared with healthy donors could be related to a significant reduction of cytokine production. Moreover, the dialytic session influenced the intrinsic antiviral activity of monocytes, favoring viral replication.
Authors: Alexander Hof; Simon Geißen; Kezia Singgih; Martin Mollenhauer; Holger Winkels; Thomas Benzing; Stephan Baldus; Friedrich Felix Hoyer Journal: Basic Res Cardiol Date: 2022-07-27 Impact factor: 12.416