BACKGROUND: The immune defect in haemodialysis (HD) patients is associated with a monocytic dysfunction, including an increased production of proinflammatory cytokines. Monocytes fall into subpopulations comprising CD14(++)CD16(-) and CD14(+)CD16(+) cells. Circulating numbers of the latter can rapidly increase during infectious episodes and inflammation. METHODS: We determined the amount of CD14(+)CD16(+) monocytes in HD patients and characterized their fate during HD treatment. In 34 HD patients and 17 healthy controls, the distinct cell populations were determined by differential blood counts and flow cytometry. Cells from 14 HD patients were analysed at the start, 10, 30 and 120 min thereafter, and at the end of HD treatment. RESULTS: Before HD, patients show a monocytosis with a strongly increased CD14(+)CD16(+) subpopulation. Early during HD treatment, circulating leukocyte numbers decrease, with monocytes being most profoundly influenced. Interestingly, among them, sequestration is most pronounced in the CD14(+) CD16(+) subpopulation. After 30 min, approximately 83+/-9% of CD14(+)CD16(+) cells are removed from circulation. This sequestration does not differ between patients treated with polyamide or haemophan membranes. The sequestration is a short-lived temporary effect and cell numbers are replenished within 120 min of treatment for the entire monocyte population. Beyond that time point, cellular activation by the dialyser membrane becomes visible. Reappearence kinetics of CD14(+)CD16(+) monocytes is slower; however, initial numbers are reached by the end of treatment. CONCLUSION: Haemodiaysis leads to temporary removal of monocytes from the bloodstream followed by the reappearance of activated cells. This might contribute to the state of chronic microinflammation, which is reflected by high levels of CD14(+)CD16(+) monocytes.
BACKGROUND: The immune defect in haemodialysis (HD) patients is associated with a monocytic dysfunction, including an increased production of proinflammatory cytokines. Monocytes fall into subpopulations comprising CD14(++)CD16(-) and CD14(+)CD16(+) cells. Circulating numbers of the latter can rapidly increase during infectious episodes and inflammation. METHODS: We determined the amount of CD14(+)CD16(+) monocytes in HDpatients and characterized their fate during HD treatment. In 34 HDpatients and 17 healthy controls, the distinct cell populations were determined by differential blood counts and flow cytometry. Cells from 14 HDpatients were analysed at the start, 10, 30 and 120 min thereafter, and at the end of HD treatment. RESULTS: Before HD, patients show a monocytosis with a strongly increased CD14(+)CD16(+) subpopulation. Early during HD treatment, circulating leukocyte numbers decrease, with monocytes being most profoundly influenced. Interestingly, among them, sequestration is most pronounced in the CD14(+) CD16(+) subpopulation. After 30 min, approximately 83+/-9% of CD14(+)CD16(+) cells are removed from circulation. This sequestration does not differ between patients treated with polyamide or haemophan membranes. The sequestration is a short-lived temporary effect and cell numbers are replenished within 120 min of treatment for the entire monocyte population. Beyond that time point, cellular activation by the dialyser membrane becomes visible. Reappearence kinetics of CD14(+)CD16(+) monocytes is slower; however, initial numbers are reached by the end of treatment. CONCLUSION: Haemodiaysis leads to temporary removal of monocytes from the bloodstream followed by the reappearance of activated cells. This might contribute to the state of chronic microinflammation, which is reflected by high levels of CD14(+)CD16(+) monocytes.
Authors: Aline Milane; Georges Khazen; Nabil Zeineddine; Mazen Amro; Leila Masri; Michella Ghassibe-Sabbagh; Sonia Youhanna; Angelique K Salloum; Marc Haber; Daniel E Platt; Jean-Baptiste Cazier; Raed Othman; Samer Kabbani; Hana Sbeite; Youssef Chami; Elie Chammas; Hamid El Bayeh; Dominique Gauguier; Antoine B Abchee; Pierre Zalloua; Antoine Barbari Journal: Int J Clin Exp Med Date: 2015-09-15
Authors: Gunnar H Heine; Alberto Ortiz; Ziad A Massy; Bengt Lindholm; Andrzej Wiecek; Alberto Martínez-Castelao; Adrian Covic; David Goldsmith; Gültekin Süleymanlar; Gérard M London; Gianfranco Parati; Rosa Sicari; Carmine Zoccali; Danilo Fliser Journal: Nat Rev Nephrol Date: 2012-03-13 Impact factor: 28.314
Authors: Eva Schepers; Erica Houthuys; Annemieke Dhondt; Grim De Meyer; Nathalie Neirynck; Pascale Bernaert; Rafael Van den Bergh; Peter Brouckaert; Raymond Vanholder; Griet Glorieux Journal: PLoS One Date: 2015-04-01 Impact factor: 3.240
Authors: Eric Seibert; Kristina Zohles; Christof Ulrich; Alexander Kluttig; Sebastian Nuding; Jan A Kors; Cees A Swenne; Karl Werdan; Roman Fiedler; Matthias Girndt Journal: BMC Cardiovasc Disord Date: 2016-11-03 Impact factor: 2.298
Authors: Elly J F Vereyken; Marina D Kraaij; Carla C Baan; Farhad Rezaee; Willem Weimar; Kathryn J Wood; Pieter J M Leenen; Ajda T Rowshani Journal: PLoS One Date: 2013-07-29 Impact factor: 3.240