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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 18181

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Dr. María Candelaria Martín-González

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Internal Medicine Department, Universidad de La Laguna, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain
Interests: liver disease; alcoholic hepatitis; liver injury; alcohol; alcohol and disease
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Emilio González-Reimers

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Guest Editor

Departamento de Medicina Interna, Servicio de Medicina Interna, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, 38320 La Laguna, Spain
Interests: specialist in internal medicine

Special Issue Information

Dear Colleagues,

Excessive ethanol consumption may cause widespread organ dysfunction, leading to a constellation of severe diseases (e.g., pancreas and/or liver function impairment, various types of cancer, cardiovascular diseases, or nutritional disorders), that markedly shorten lifespan. An important mechanism underlying health derangement in excessive drinkers includes an enhanced inflammatory response, mainly triggered by ethanol/acetaldehyde-mediated bacterial overload in portal blood, and by the increased oxidative damage provoked by ethanol metabolism and acetaldehyde adducts. However, our knowledge regarding the proinflammatory effects of alcoholism is still incomplete, and that regarding the therapeutic role of antioxidants or cytokine-blocking agents is disappointing. Therefore, research is still needed in this field.

This Special Issue aims to provide a platform for molecular mechanistic research on alcohol-induced inflammation, with a special focus on potential treatments and novel pathogenic pathways involved in inflammatory disease. We warmly welcome your submissions of original papers and reviews based on results from molecular viewpoints.

Dr. María Candelaria Martín-González
Prof. Dr. Emilio González-Reimers
Guest Editors

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Keywords

alcohol
inflammation
alcohol use disorder
alcoholic liver disease
liver disease
alcoholic hepatitis
liver injury
oxidative damage

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Published Papers (7 papers)

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Research

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16 pages, 6258 KiB

Open AccessArticle

Prenatal Alcohol Exposure Disrupts CXCL16 Expression in Rat Hippocampus: Temporal and Sex Differences

by Mayra Madeleine Padilla-Valdez, Margarita Belem Santana-Bejarano, Marisol Godínez-Rubí, Daniel Ortuño-Sahagún and Argelia Esperanza Rojas-Mayorquín

Int. J. Mol. Sci. 2025, 26(5), 1920; https://doi.org/10.3390/ijms26051920 - 23 Feb 2025

Viewed by 890

Abstract

Prenatal alcohol exposure (PAE) affects around 40,000 newborns every year and poses a significant health risk. Although much is already known about the neurotoxic mechanisms of PAE, new findings continue to emerge. Studies with mouse models show that PAE leads to overexpression of proinflammatory cytokines and chemokines in the brain, which disrupts important neurodevelopmental processes such as cell migration, survival and proliferation of neurons. The chemokine CXCL16 is overexpressed in the brain following various impairments, including PAE. This study shows that CXCL16 expression varies by developmental stage and sex, consistent with known sexual dimorphism in immune responses. In females, CXCL16 expression may be influenced by estrogen-related mechanisms, possibly related to the alcohol-mediated rebound effect described here. In contrast, the male hippocampus shows greater resilience to PAE-induced CXCL16 changes. Furthermore, the presence of CXCL16 in neuronal nuclei suggests a role in gene regulation, similar to other chemokines such as CCL5 and CXCL4. These findings shed light on the role of chemokines in hippocampal neuroplasticity and may pave the way for better treatment of fetal alcohol spectrum disorder (FASD). Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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16 pages, 2559 KiB

Open AccessArticle

Role of Myeloid Cell-Specific Adenylyl Cyclase Type 7 in Lipopolysaccharide- and Alcohol-Induced Immune Responses

by Yawen Hu, Sonika Patial, Yogesh Saini and Masami Yoshimura

Int. J. Mol. Sci. 2024, 25(23), 12831; https://doi.org/10.3390/ijms252312831 - 28 Nov 2024

Viewed by 839

Abstract

Clinical and experimental evidence indicates that alcohol use causes various abnormalities in the immune system and compromises immune functions. However, the mechanistic understanding of ethanol’s effects on the immune system remains limited. Cyclic AMP (cAMP) regulates multiple processes, including immune responses. Earlier research indicated that type 7 adenylyl cyclase (AC7) regulates the immune system and is highly responsive to ethanol. Therefore, we hypothesized that AC7 is a central player in regulating the effects of alcohol on innate immune responses. To test this hypothesis, we utilized a myeloid lineage-specific AC7 KO mouse model and compared the effects of acute and chronic ethanol treatment on their innate immune responses induced by systemic lipopolysaccharide (LPS) challenge. Our results demonstrate that AC7 KO mice had significantly lower survival rates under LPS challenge. Chronic ethanol consumption rescued AC7 KO mice from LPS-induced death. AC7 KO and ethanol, acute and chronic, affected several measurements of cytokine mRNA expressions, including IL-1β, TNFα, IL-6, and IL-10 in the lung and liver. In a few cases, statistical analysis indicated that these two factors interacted, suggesting that AC7 played some role in ethanol’s effect on cytokine expression. Thus, this study demonstrated AC7’s role in ethanol’s effect on the innate immune response. Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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19 pages, 2551 KiB

Open AccessArticle

Altered Expression of Neuroplasticity-Related Genes in Alcohol Addiction and Treatment

by Evangelia Legaki, Nikolas Dovrolis, Nikoletta Moscholiou, Ilias Koutromanos, Efthimios Vassilopoulos, Antonios Dakanalis, Maria Gazouli and Elias Tzavellas

Int. J. Mol. Sci. 2024, 25(21), 11349; https://doi.org/10.3390/ijms252111349 - 22 Oct 2024

Cited by 2 | Viewed by 1737

Abstract

Alcohol use disorder’s complexity arises from genetic and environmental factors, with alcohol metabolism genes and neurotransmitter pathways being critical. This study aims to analyze synaptic plasticity gene expression changes in individuals with AUD in order to study their contribution to AUD development and to identify potential biomarkers of treatment response. RNA was extracted from whole peripheral blood (20 patients, 10 healthy controls), before and after treatment (Qiagen AllPrep RNA/DNA Mini Kit), and the gene expression of 84 genes related to neuroplasticity was studied using the RT2 Profiler for Human Synaptic Plasticity RT-PCR Array (PAHS-126ZA, Qiagen), comparing AUD patients to control and responders to non-responders. The potential prognostic/predictive biomarkers were searched using machine learning models. A total of 35 dysregulated genes were found in AUD patients. EPHB2, EGR, and AKT1 were increased, while TIMP1, NCAM1, and GRM2 were decreased. Responders showed distinct gene expression profiles at baseline. After treatment, the expression of 57 genes was normalized, while NCAM1, GRM2, and BDNF showed the most significant recovery. EGR4, INHBA, and NCAM1 emerged as potential biomarkers to predict treatment success. These results indicate that gene profiles in peripheral blood can serve as prognostic markers for the prognosis and treatment of AUD, although further validation is required. Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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17 pages, 12015 KiB

Open AccessArticle

N-3 Polyunsaturated Fatty Acids Protect against Alcoholic Liver Steatosis by Activating FFA4 in Kupffer Cells

by Saeromi Kang, Jung-Min Koh and Dong-Soon Im

Int. J. Mol. Sci. 2024, 25(10), 5476; https://doi.org/10.3390/ijms25105476 - 17 May 2024

Cited by 2 | Viewed by 1630

Abstract

Supplementation with fish oil rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs) effectively reduces acute and chronic alcohol-induced hepatic steatosis. We aimed to find molecular mechanisms underlying the effects of n-3 PUFAs in alcohol-induced hepatic steatosis. Because free fatty acid receptor 4 (FFA4, also known as GPR120) has been found as a receptor for n-3 PUFAs in an ethanol-induced liver steatosis model, we investigated whether n-3 PUFAs protect against liver steatosis via FFA4 using AH7614, an FFA4 antagonist, and Ffa4 knockout (KO) mice. N-3 PUFAs and compound A (CpdA), a selective FFA4 agonist, reduced the ethanol-induced increase in lipid accumulation in hepatocytes, triglyceride content, and serum ALT levels, which were not observed in Ffa4 KO mice. N-3 PUFAs and CpdA also reduced the ethanol-induced increase in lipogenic sterol regulatory element-binding protein-1c expression in an FFA4-dependent manner. In Kupffer cells, treatment with n-3 PUFA and CpdA reversed the ethanol-induced increase in tumor necrosis factor-α, cyclooxygenase-2, and NLR family pyrin domain-containing 3 expression levels in an FFA4-dependent manner. In summary, n-3 PUFAs protect against ethanol-induced hepatic steatosis via the anti-inflammatory actions of FFA4 on Kupffer cells. Our findings suggest FFA4 as a therapeutic target for alcoholic hepatic steatosis. Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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14 pages, 787 KiB

Open AccessArticle

Sarcopenic Obesity in People with Alcoholic Use Disorder: Relation with Inflammation, Vascular Risk Factors and Serum Vitamin D Levels

by Candelaria Martín-González, Paula Fernández-Alonso, Onán Pérez-Hernández, Pedro Abreu-González, Elisa Espelosín-Ortega, Camino María Fernández-Rodríguez, Esther Martín-Ponce and Emilio González-Reimers

Int. J. Mol. Sci. 2023, 24(12), 9976; https://doi.org/10.3390/ijms24129976 - 9 Jun 2023

Cited by 10 | Viewed by 2284

Abstract

In recent years, the terms sarcopenia, sarcopenic obesity, and osteosarcopenic obesity (OSO) were coined to define a situation in elderly people strongly associated with frailty and increased mortality. Possibly, a complex interplay of several hormones and cytokines are involved in its development. Ongoing research detected that OSO may occur at any age and in several conditions. The prevalence of OSO in alcoholism was poorly analyzed. The aim of this study was to analyze the prevalence of OSO in alcoholism and its relationship with proinflammatory cytokines and/or common complications of alcoholism, such as cirrhosis, cancer, or vascular disease. We included 115 patients with alcoholic use disorder. Body composition analysis was performed by double X-ray absorptiometry. Handgrip strength was recorded using a dynamometer. We assessed liver function according to Child’s classification, and determined serum levels of proinflammatory cytokines (TNF-α, IL-6, IL-8), routine laboratory variables, and vitamin D. People with alcoholic use disorder showed a high prevalence of OSO, especially regarding OSO obesity (60%), OSO osteopenia (55.65%), and OSO lean mass (60.17%). OSO handgrip was closely, independently, related to the presence of vascular calcification (χ² = 17.00; p < 0.001). OSO handgrip was related to several proinflammatory cytokines and vitamin D. Vitamin D deficiency kept a close correlation with OSO handgrip (rho = −0.54, p < 0.001). Therefore, among people with alcohol use disorder, OSO prevalence was high. OSO handgrip is related to serum proinflammatory cytokine levels supporting the possible pathogenetic role of these cytokines on OSO development. Vitamin D deficiency is related to OSO handgrip suggesting its pathogenetic involvement in sarcopenia in patients with alcohol use disorder. The close association between OSO handgrip and vascular calcification is clinically relevant and suggests that OSO handgrip may constitute a prognostic tool in these patients. Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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19 pages, 4555 KiB

Open AccessArticle

Potential Benefits of Epidermal Growth Factor for Inhibiting Muscle Degrative Markers in Rats with Alcoholic Liver Damage

by Qian Xiao, Yi-Hsiu Chen, Ya-Ling Chen, Yu-Shan Chien, Li-Hsuan Hsieh, Hitoshi Shirakawa and Suh-Ching Yang

Int. J. Mol. Sci. 2023, 24(10), 8845; https://doi.org/10.3390/ijms24108845 - 16 May 2023

Cited by 1 | Viewed by 1900

Abstract

This study investigated the beneficial effects of epidermal growth factor (EGF) on muscle loss in rats with chronic ethanol feeding. Six-week-old male Wistar rats were fed either a control liquid diet without EGF (C group, n = 12) or EGF (EGF-C group, n = 18) for two weeks. From the 3rd to 8th week, the C group was divided into two groups. One was continually fed with a control liquid diet (C group), and the other one was fed with an ethanol-containing liquid diet (E group); moreover, the EGF-C group was divided into three groups, such as the AEGF-C (continually fed with the same diet), PEGF-E (fed with the ethanol-containing liquid diet without EGF), and AEGF-E (fed with the ethanol-containing liquid diet with EGF). As a result, the E group had significantly higher plasma ALT and AST, endotoxin, ammonia, and interleukin 1b (IL-1b) levels, along with liver injuries, such as hepatic fatty changes and inflammatory cell infiltration. However, plasma endotoxin and IL-1b levels were significantly decreased in the PEGF-E and AEGF-E groups. In addition, the protein level of muscular myostatin and the mRNA levels of forkhead box transcription factors (FOXO), muscle RING-finger protein-1 (MURF-1) and atorgin-1 was increased considerably in the E group but inhibited in the PEGF-E and AEGF-E groups. According to the principal coordinate analysis findings, the gut microbiota composition differed between the control and ethanol liquid diet groups. In conclusion, although there was no noticeable improvement in muscle loss, EGF supplementation inhibited muscular protein degradation in rats fed with an ethanol-containing liquid diet for six weeks. The mechanisms might be related to endotoxin translocation inhibition, microbiota composition alteration as well as the amelioration of liver injury. However, the reproducibility of the results must be confirmed in future studies. Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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Review

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13 pages, 3805 KiB

Open AccessReview

Alcohol, Inflammation, and Microbiota in Alcoholic Liver Disease

by Marija Dukić, Tijana Radonjić, Igor Jovanović, Marija Zdravković, Zoran Todorović, Nemanja Kraišnik, Bojana Aranđelović, Olga Mandić, Višeslav Popadić, Novica Nikolić, Slobodan Klašnja, Andrea Manojlović, Anica Divac, Jasna Gačić, Milica Brajković, Svetlana Oprić, Maja Popović and Marija Branković

Int. J. Mol. Sci. 2023, 24(4), 3735; https://doi.org/10.3390/ijms24043735 - 13 Feb 2023

Cited by 84 | Viewed by 7570

Abstract

Alcoholic liver disease (ALD) is a consequence of excessive alcohol use. According to many studies, alcohol represents a significant socioeconomic and health risk factor in today’s population. According to data from the World Health Organization, there are about 75 million people who have alcohol disorders, and it is well known that its use leads to serious health problems. ALD is a multimodality spectrum that includes alcoholic fatty liver disease (AFL) and alcoholic steatohepatitis (ASH), consequently leading to liver fibrosis and cirrhosis. In addition, the rapid progression of alcoholic liver disease can lead to alcoholic hepatitis (AH). Alcohol metabolism produces toxic metabolites that lead to tissue and organ damage through an inflammatory cascade that includes numerous cytokines, chemokines, and reactive oxygen species (ROS). In the process of inflammation, mediators are cells of the immune system, but also resident cells of the liver, such as hepatocytes, hepatic stellate cells, and Kupffer cells. These cells are activated by exogenous and endogenous antigens, which are called pathogen and damage-associated molecular patterns (PAMPs, DAMPs). Both are recognized by Toll-like receptors (TLRs), which activation triggers the inflammatory pathways. It has been proven that intestinal dysbiosis and disturbed integrity of the intestinal barrier perform a role in the promotion of inflammatory liver damage. These phenomena are also found in chronic excessive use of alcohol. The intestinal microbiota has an important role in maintaining the homeostasis of the organism, and its role in the treatment of ALD has been widely investigated. Prebiotics, probiotics, postbiotics, and symbiotics represent therapeutic interventions that can have a significant effect on the prevention and treatment of ALD. Full article

(This article belongs to the Special Issue Alcohol and Inflammation)

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