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Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers

BACKGROUND: Alcohol drinking is associated with a serious risk of developing health problems as well as with a large number of traumatic injuries. Although chronic alcohol misuse is known to contribute to severe inflammatory complications, the effects of an acute alcohol misuse are still unclear. He...

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Autores principales: Haag, Florian, Janicova, Andrea, Xu, Baolin, Powerski, Maciej, Fachet, Melanie, Bundkirchen, Katrin, Neunaber, Claudia, Marzi, Ingo, Relja, Borna, Sturm, Ramona
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360092/
https://www.ncbi.nlm.nih.gov/pubmed/33783566
http://dx.doi.org/10.1007/s00068-021-01643-x
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author Haag, Florian
Janicova, Andrea
Xu, Baolin
Powerski, Maciej
Fachet, Melanie
Bundkirchen, Katrin
Neunaber, Claudia
Marzi, Ingo
Relja, Borna
Sturm, Ramona
author_facet Haag, Florian
Janicova, Andrea
Xu, Baolin
Powerski, Maciej
Fachet, Melanie
Bundkirchen, Katrin
Neunaber, Claudia
Marzi, Ingo
Relja, Borna
Sturm, Ramona
author_sort Haag, Florian
collection PubMed
description BACKGROUND: Alcohol drinking is associated with a serious risk of developing health problems as well as with a large number of traumatic injuries. Although chronic alcohol misuse is known to contribute to severe inflammatory complications, the effects of an acute alcohol misuse are still unclear. Here, the impact of acute alcohol drinking on leukocyte counts and their cellular functions were studied. METHODS: Twenty-two healthy volunteers (12 female, 10 male) received a predefined amount of a whiskey-cola mixed drink (40% v/v), at intervals of 20 min, over 4 h to achieve a blood alcohol concentration of 1‰. Blood samples were taken before drinking T(0), 2 h (T(2)), 4 h (T(4)), 6 h (T(6)), 24 h (T(24)) and 48 h (T(48)) after starting drinking alcohol. Leukocytes, monocytes and granulocyte counts and their functions regarding the production of reactive oxidative species (ROS), phagocytosis and apoptosis were analyzed by flow cytometry. RESULTS: Total leukocyte counts significantly increased at T(2) and T(4), while granulocyte and monocyte counts decreased at T(4) and T(6) vs. T(0). Monocytes increased significantly at T(24) and T(48) vs. T(0). While the total number of ROS-producing leukocytes and notably granulocytes significantly increased, in parallel, the intracellular ROS intensity decreased at T(2) and T(6). The numbers of ROS-positive monocytes have shown a delayed modulation of ROS, with a significant reduction in the total number of ROS-producing cells at T(48) and a significantly reduced intracellular ROS-intensity at T(24). Phagocyting capacity of leukocytes significantly decreased at T(4) and T(6). In general leukocytes, and notably granulocytes demonstrated significantly increased early (T(2)), while monocyte exerted significantly increased late apoptosis (T(24) and T(48)). CONCLUSIONS: Alcohol drinking immediately impacts leukocyte functions, while the impact on monocytes occurs at even later time points. Thus, even in young healthy subjects, alcohol drinking induces immunological changes that are associated with diminished functions of innate immune cells that persist for days.
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spelling pubmed-93600922022-08-10 Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers Haag, Florian Janicova, Andrea Xu, Baolin Powerski, Maciej Fachet, Melanie Bundkirchen, Katrin Neunaber, Claudia Marzi, Ingo Relja, Borna Sturm, Ramona Eur J Trauma Emerg Surg Original Article BACKGROUND: Alcohol drinking is associated with a serious risk of developing health problems as well as with a large number of traumatic injuries. Although chronic alcohol misuse is known to contribute to severe inflammatory complications, the effects of an acute alcohol misuse are still unclear. Here, the impact of acute alcohol drinking on leukocyte counts and their cellular functions were studied. METHODS: Twenty-two healthy volunteers (12 female, 10 male) received a predefined amount of a whiskey-cola mixed drink (40% v/v), at intervals of 20 min, over 4 h to achieve a blood alcohol concentration of 1‰. Blood samples were taken before drinking T(0), 2 h (T(2)), 4 h (T(4)), 6 h (T(6)), 24 h (T(24)) and 48 h (T(48)) after starting drinking alcohol. Leukocytes, monocytes and granulocyte counts and their functions regarding the production of reactive oxidative species (ROS), phagocytosis and apoptosis were analyzed by flow cytometry. RESULTS: Total leukocyte counts significantly increased at T(2) and T(4), while granulocyte and monocyte counts decreased at T(4) and T(6) vs. T(0). Monocytes increased significantly at T(24) and T(48) vs. T(0). While the total number of ROS-producing leukocytes and notably granulocytes significantly increased, in parallel, the intracellular ROS intensity decreased at T(2) and T(6). The numbers of ROS-positive monocytes have shown a delayed modulation of ROS, with a significant reduction in the total number of ROS-producing cells at T(48) and a significantly reduced intracellular ROS-intensity at T(24). Phagocyting capacity of leukocytes significantly decreased at T(4) and T(6). In general leukocytes, and notably granulocytes demonstrated significantly increased early (T(2)), while monocyte exerted significantly increased late apoptosis (T(24) and T(48)). CONCLUSIONS: Alcohol drinking immediately impacts leukocyte functions, while the impact on monocytes occurs at even later time points. Thus, even in young healthy subjects, alcohol drinking induces immunological changes that are associated with diminished functions of innate immune cells that persist for days. Springer Berlin Heidelberg 2021-03-30 2022 /pmc/articles/PMC9360092/ /pubmed/33783566 http://dx.doi.org/10.1007/s00068-021-01643-x Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Article
Haag, Florian
Janicova, Andrea
Xu, Baolin
Powerski, Maciej
Fachet, Melanie
Bundkirchen, Katrin
Neunaber, Claudia
Marzi, Ingo
Relja, Borna
Sturm, Ramona
Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
title Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
title_full Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
title_fullStr Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
title_full_unstemmed Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
title_short Reduced phagocytosis, ROS production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
title_sort reduced phagocytosis, ros production and enhanced apoptosis of leukocytes upon alcohol drinking in healthy volunteers
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360092/
https://www.ncbi.nlm.nih.gov/pubmed/33783566
http://dx.doi.org/10.1007/s00068-021-01643-x
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