Peripheral cellular immune alterations during excessive alcohol consumption

Introduction and Objectives: The mechanisms that participate in the pathophysiology of chronic alcohol consumption and Alcoholic Liver Disease (ALD) include alterations of the innate and adaptive immune system, until now there is little information about the damage inducing mechanisms and their part...

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Main Authors: Karla Z. Medina-Avila, Abigail Hernandez-Barragan, Marisela Hernández-Santillan, Isabel Villagómez-López, Adrián Flores-Sanchez, Melanie Acosta-Gutiérrez, Viridiana Bautista-Nava, Isaac B Flores-Islas, Jesús A Dorantes-Álvarez, Moisés Martinez-Castillo, Fátima Higuera-de la Tijera, José L Pérez-Hernández, Gabriela Gutiérrez-Reyes
Format: Article
Language:English
Published: Elsevier 2025-04-01
Series:Annals of Hepatology
Online Access:http://www.sciencedirect.com/science/article/pii/S1665268125000717
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author Karla Z. Medina-Avila
Abigail Hernandez-Barragan
Marisela Hernández-Santillan
Isabel Villagómez-López
Adrián Flores-Sanchez
Melanie Acosta-Gutiérrez
Viridiana Bautista-Nava
Isaac B Flores-Islas
Jesús A Dorantes-Álvarez
Moisés Martinez-Castillo
Fátima Higuera-de la Tijera
José L Pérez-Hernández
Gabriela Gutiérrez-Reyes
author_facet Karla Z. Medina-Avila
Abigail Hernandez-Barragan
Marisela Hernández-Santillan
Isabel Villagómez-López
Adrián Flores-Sanchez
Melanie Acosta-Gutiérrez
Viridiana Bautista-Nava
Isaac B Flores-Islas
Jesús A Dorantes-Álvarez
Moisés Martinez-Castillo
Fátima Higuera-de la Tijera
José L Pérez-Hernández
Gabriela Gutiérrez-Reyes
author_sort Karla Z. Medina-Avila
collection DOAJ
description Introduction and Objectives: The mechanisms that participate in the pathophysiology of chronic alcohol consumption and Alcoholic Liver Disease (ALD) include alterations of the innate and adaptive immune system, until now there is little information about the damage inducing mechanisms and their participation in the development of the disease. The objective was to determine the imbalance of peripheral cellular immunity according to the pattern of alcohol consumption. Materials and Patients: Cross-sectional study included 5 groups of subjects with different patterns of alcohol consumption using AUDIT and DSM-IV. G1: Control with OH consumption<10g/day (CT); G2: Risk (Ri) and G3: Abuse (A) with AUDIT>8; G4: Alcoholism, without clinical or biochemical stigmata of damage (OH); G5: Patients with alcoholic liver cirrhosis (CiOH). T cells, T-CD4+, T-CD8+, B cells, NK and NKT were determined in peripheral blood by flow cytometry. For statistical analysis we performed U-Mann Whitney, considering p<0.05 significant. Results: In the study, 589 subjects were included, average age 32±11, 30±11, 23±3, 31.5±13 and 47.5±7.7 years CT, Ri, A, OH y CiOH respectively (p<0.001). Alcohol consumption (g/day) was higher in OH 158(210,107), and CiOH 293(340,246) (p<0.001,both). Cellular determination of NK we found elevated (15.4 and 13.3vs11.1) and NKT (3.7 and 2.5vs1.7) in groups A, OH and CiOH (p<0.001), (p<0.001), (p<0.05) only in NK, during CiOH NKT decrease (1.4vs1.7)(p<0.001). In T cells we observed a decrease in OH (62.3vs66.5) and CiOH (56.8vs66.5) (p<0.001), the percentage of CD4+ cells decreased from the Ri group (35.7vs38.8)(p<0.01) until OH (35.1vs38.8)(p<0.01) while during CiOH they increase (41.8vs35.1)(p<0.05). CD8+ cells increase during OH (24.5vs21.1)(p<0.05) and decrease in CiOH (13.9vs21.1)(p<0.001) respectively. Conclusions: The immune abnormalities presented during risky consumption, abuse, dependence and cirrhosis due to alcohol are differential, the most significant changes are observed in the cytotoxic NK, NKT and CD8+ and regulatory CD4+ populations generating a cellular imbalance that could be related to development and progression of liver damage.
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spelling doaj-art-bc6121e56a2e4b69b6302a91389bc9f82025-08-20T02:13:48ZengElsevierAnnals of Hepatology1665-26812025-04-013010184710.1016/j.aohep.2025.101847Peripheral cellular immune alterations during excessive alcohol consumptionKarla Z. Medina-Avila0Abigail Hernandez-Barragan1Marisela Hernández-Santillan2Isabel Villagómez-López3Adrián Flores-Sanchez4Melanie Acosta-Gutiérrez5Viridiana Bautista-Nava6Isaac B Flores-Islas7Jesús A Dorantes-Álvarez8Moisés Martinez-Castillo9Fátima Higuera-de la Tijera10José L Pérez-Hernández11Gabriela Gutiérrez-Reyes12Liver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoGastroenterology and Hepatology Department. General Hospital of Mexico “Dr. Eduardo Liceaga”, MéxicoGastroenterology and Hepatology Department. General Hospital of Mexico “Dr. Eduardo Liceaga”, MéxicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoIntroduction and Objectives: The mechanisms that participate in the pathophysiology of chronic alcohol consumption and Alcoholic Liver Disease (ALD) include alterations of the innate and adaptive immune system, until now there is little information about the damage inducing mechanisms and their participation in the development of the disease. The objective was to determine the imbalance of peripheral cellular immunity according to the pattern of alcohol consumption. Materials and Patients: Cross-sectional study included 5 groups of subjects with different patterns of alcohol consumption using AUDIT and DSM-IV. G1: Control with OH consumption<10g/day (CT); G2: Risk (Ri) and G3: Abuse (A) with AUDIT>8; G4: Alcoholism, without clinical or biochemical stigmata of damage (OH); G5: Patients with alcoholic liver cirrhosis (CiOH). T cells, T-CD4+, T-CD8+, B cells, NK and NKT were determined in peripheral blood by flow cytometry. For statistical analysis we performed U-Mann Whitney, considering p<0.05 significant. Results: In the study, 589 subjects were included, average age 32±11, 30±11, 23±3, 31.5±13 and 47.5±7.7 years CT, Ri, A, OH y CiOH respectively (p<0.001). Alcohol consumption (g/day) was higher in OH 158(210,107), and CiOH 293(340,246) (p<0.001,both). Cellular determination of NK we found elevated (15.4 and 13.3vs11.1) and NKT (3.7 and 2.5vs1.7) in groups A, OH and CiOH (p<0.001), (p<0.001), (p<0.05) only in NK, during CiOH NKT decrease (1.4vs1.7)(p<0.001). In T cells we observed a decrease in OH (62.3vs66.5) and CiOH (56.8vs66.5) (p<0.001), the percentage of CD4+ cells decreased from the Ri group (35.7vs38.8)(p<0.01) until OH (35.1vs38.8)(p<0.01) while during CiOH they increase (41.8vs35.1)(p<0.05). CD8+ cells increase during OH (24.5vs21.1)(p<0.05) and decrease in CiOH (13.9vs21.1)(p<0.001) respectively. Conclusions: The immune abnormalities presented during risky consumption, abuse, dependence and cirrhosis due to alcohol are differential, the most significant changes are observed in the cytotoxic NK, NKT and CD8+ and regulatory CD4+ populations generating a cellular imbalance that could be related to development and progression of liver damage.http://www.sciencedirect.com/science/article/pii/S1665268125000717
spellingShingle Karla Z. Medina-Avila
Abigail Hernandez-Barragan
Marisela Hernández-Santillan
Isabel Villagómez-López
Adrián Flores-Sanchez
Melanie Acosta-Gutiérrez
Viridiana Bautista-Nava
Isaac B Flores-Islas
Jesús A Dorantes-Álvarez
Moisés Martinez-Castillo
Fátima Higuera-de la Tijera
José L Pérez-Hernández
Gabriela Gutiérrez-Reyes
Peripheral cellular immune alterations during excessive alcohol consumption
Annals of Hepatology
title Peripheral cellular immune alterations during excessive alcohol consumption
title_full Peripheral cellular immune alterations during excessive alcohol consumption
title_fullStr Peripheral cellular immune alterations during excessive alcohol consumption
title_full_unstemmed Peripheral cellular immune alterations during excessive alcohol consumption
title_short Peripheral cellular immune alterations during excessive alcohol consumption
title_sort peripheral cellular immune alterations during excessive alcohol consumption
url http://www.sciencedirect.com/science/article/pii/S1665268125000717
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