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. 2021 Jul 1;11:13690. doi: 10.1038/s41598-021-93086-y

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© The Author(s) 2021

Open Access This 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/.

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CD14⁺CD16⁻ monocytes in alcohol-dependent (AD) patients with ADH1B*2 and ALDH2*1/*2 genotypes demonstrate a deeply suppressed phenotype. (A–C) Concentration of TNF-α in the culture supernatants of CD14⁺ monocytes isolated from AD patients on admission (A) and at 4 weeks post-abstinence (B) according to the genetic polymorphism of ADH1B (upper), ALDH2 (middle), and the combination (lower). (C) Frequency of CD14⁺CD16⁻ monocytes isolated from AD patients on admission according to the genetic polymorphism in ADH1B (upper), ALDH2 (middle), and the combination (lower). Data represent the mean ± SD. *p < 0.05 by Student’s paired t-test for two groups or by one-way ANOVA for three or four groups. N.S.: not significant.