Effects of probiotics on liver function, inflammation, and gut microbiota in alcoholic liver injury: a systematic review and meta-analysis

Purpose: This systematic review and meta-analysis aimed to evaluate the effects of probiotic supplementation on alcohol metabolism, liver function biomarkers, inflammatory indicators, and gut microbiota composition in patients with alcoholic liver disease (ALD), providing insights into their potential therapeutic role.

Methods: A comprehensive search of the PubMed, Scopus, Web of Science, and Cochrane Library databases identified clinical studies assessing probiotic interventions in adults with ALD.

Results: A total of 12 clinical trials conducted between 2008 and 2025 were included. Probiotic supplementation resulted in significant reductions in liver enzymes, including ALT (WMD = −10.10; 95% CI: −15.34, −4.87) and AST (WMD = −13.05; 95% CI: −21.33, −4.78). No significant effects were observed for GGT or ALP. Probiotics did not significantly influence blood alcohol or acetaldehyde levels. Regarding inflammatory markers, probiotics did not significantly affect LPS, TNF-α, IL-1β, or IL-6, and IL-10. Microbial analyses showed an increase in beneficial gut bacteria, including Lactobacillus, Bifidobacterium, Faecalibacterium, and Prevotella, and a decrease in pathogenic taxa such as Escherichia and Shigella.

Conclusion: Probiotic supplementation shows promising benefits for improving liver enzyme profiles and modulating the gut microbiota in patients with ALD. However, inconsistent effects on markers of inflammation and alcohol metabolism highlight the need for large-scale, high-quality randomized trials to confirm the therapeutic potential of probiotics in ALD.

Introduction

Global alcohol consumption has risen significantly, contributing to over 2.6 million deaths annually in 2019, approximately 4.7% of all global mortality (1). Young adults are particularly impacted; for instance, 13% of alcohol-attributable deaths occur among individuals aged 20 to 39 (2). Alcoholic liver disease (ALD) is a major cause of chronic liver injury and is responsible for nearly half of all liver-related deaths worldwide (3). These patterns often reflect broader socioeconomic shifts, including increased alcohol availability driven by economic growth and changing social norms (4).

Seminal studies first identified elevated levels of bacterial endotoxin (lipopolysaccharide, LPS) in the portal circulation of patients with ALD, implicating intestinal barrier dysfunction in the pathogenesis of liver inflammation (5). Chronic ethanol exposure disrupts gut–liver homeostasis, permitting translocation of microbial products that activate hepatic immune responses (6).

The gut–liver axis plays a pivotal role in maintaining liver health, and chronic alcohol intake significantly impairs this balance (7). Alcohol abuse causes an imbalance in the gut microbiome, characterized by a decrease in beneficial bacteria and an increase in harmful organisms (8). Specifically, ALD is consistently linked to a reduction in anti-inflammatory, short-chain fatty acid (SCFA)–producing bacteria such as Faecalibacterium, Roseburia, Ruminococcus, and other members of the Firmicutes and Bacteroidetes phyla (9, 10). On the other hand, there is an overgrowth of potentially harmful Enterobacteriaceae, including Escherichia, Shigella, and Klebsiella, as well as a higher abundance of Enterococcus (10, 11). These microbial shifts reduce overall gut diversity and compromise the integrity of the mucosal barrier.

Probiotic supplements have shown therapeutic promise in treating ALD by influencing the gut–liver axis (12). Multiple strains have been studied in both laboratory and early clinical trials. Notably, Lactobacillus strains, such as L. rhamnosus GG, L. casei, L. plantarum, and L. helveticus, along with Bifidobacterium strains like B. bifidum, and spore-forming species like Clostridium butyricum, have been studied (10–12). These probiotics help restore gut balance disrupted by alcohol by increasing beneficial bacteria such as Lactobacilli and Bifidobacteria, while reducing harmful gram-negative bacteria like Escherichia coli (13). Meta-analyses indicate that probiotic supplementation can reduce intestinal endotoxemia, restore microbial balance, and attenuate hepatic inflammation (14, 15). Collectively, these effects support their utility as a promising adjunct therapy for ALD.

To provide a comprehensive synthesis of clinical evidence on the efficacy of probiotics in ALD, with particular focus on their impacts on alcohol metabolic parameters, hepatic function biomarkers, systemic inflammation, and gut microbiota alterations. This study aims to systematically evaluate the effects of probiotic supplementation on alcohol metabolism parameters, hepatic function, inflammatory markers, and gut microbiota profiles in individuals with ALD through a meta-analysis of clinical trials. By integrating these methodologies, this review seeks to provide comprehensive insights into the therapeutic potential of probiotics in ALD and identify priorities for future clinical research.

Methods

Study design

The study was conducted as a systematic review and meta-analysis following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (16).

Eligibility criteria

Clinical trials evaluating the effects of probiotics supplementation on alcoholic liver injury or alcoholic liver disease were included. Observational studies, review articles, and non-randomized trials were excluded. The PICO framework was used to determine the inclusion criteria. Participants (P) of patients who were newly diagnosed with alcoholic liver injury or alcoholic liver disease of both genders were included. The intervention (I) was probiotics supplementation at any dosage and duration. Comparators (C) included a placebo, no intervention. Outcomes (O) were changes in alcohol metabolism, liver function, inflammatory biomarkers, and gut microbiota.

Search strategy

A comprehensive search was conducted in electronic databases, including PubMed, Scopus, Web of Science, and Cochrane Library, from inception to October 2025. The search strategy combined keywords and Medical Subject Headings (MeSH) related to “probiotics,” “alcoholic liver disease,” and “alcohol metabolism.” The full search strategy is provided in Supplementary File. No language restrictions were applied.

Study selection

Search records were uploaded into a reference manager and de-duplicated. Two reviewers independently screened titles and abstracts to identify potentially eligible studies. Full-text articles were then evaluated against the predefined inclusion criteria, with any disagreements resolved through consultation with a third reviewer. The study selection process was reported using a PRISMA flow diagram.

Data extraction

Two reviewers independently extracted data using a standardized form, recording key information such as study characteristics (author, publication year, location, and design), participant details (sample size and age), intervention features (probiotic dose, duration, and strains), and outcome measures (mean ± standard deviation [SD] changes). Any differences between reviewers were resolved by consensus.

Risk of bias assessment

The methodological quality of included studies was assessed using the Cochrane Risk of Bias tool (17). Each domain was rated as “low,” “unclear,” or “high risk” of bias. Two reviewers independently conducted the assessments, and any disagreements were resolved through discussion with a third reviewer.

Statistical analysis

Statistical analyses were performed using Stata Statistical Software, version 14 (StataCorp, College Station, TX, USA), with a random-effects model employed to pool the data. Weighted mean differences (WMDs) and their corresponding 95% confidence intervals (CIs) were calculated to estimate the overall effect sizes (18). Heterogeneity among studies was assessed using the I² statistic, with values greater than 50% indicating substantial heterogeneity (19). Sensitivity analyses were conducted using the leave-one-out method to evaluate the influence of individual studies on the pooled results (20). Publication bias was assessed visually through funnel plots and statistically using Begg’s and Egger’s tests. In cases of detected publication bias, trim-and-fill analysis was applied. Statistical significance was defined as a p-value < 0.05 for all analyses.

Results

Characteristics of included studies

The PRISMA flowchart (Figure 1) systematically illustrates the study selection process. Out of 2,745 records initially identified, 974 duplicates were removed, and 1,748 studies were excluded after title and abstract screening. Ultimately, 23 full-text articles were assessed for eligibility. A total of 12 clinical trials conducted between 2008 and 2025 were included, covering participant groups from Korea, China, Russia, Japan, the United States, and the United Kingdom (10–12, 21–29) (Table 1). Sample sizes ranged from 20 to 158 individuals, and the distribution of participants across probiotic and control groups varied by study design. Participants consisted of adults aged 18 to 65 years, including both males and females (with males comprising 55–75%), exhibiting disease severity from mild to moderate ALD; a limited number of studies encompassed individuals with more advanced liver injury. The studies investigated a broad spectrum of probiotic preparations, including Lacticaseibacillus rhamnosus R0011, Lactobacillus helveticus R005, Bifidobacterium bifidum, Lactobacillus plantarum 8PA3, Weizmannia coagulans BC99, Lactobacillus casei Shirota, Lactobacillus gasseri, Bifidobacterium lactis, Bifidobacterium breve, and various multi-strain formulations. Intervention periods ranged from 1 to 8 weeks, representing both short-term and mid-term probiotic administration. Across the included trials, commonly reported outcomes comprised liver enzyme markers: ALT, AST, GGT, and ALP, and inflammatory biomarkers such as TNF-α, IL-6, IL-10, IL-1β, as well as lipopolysaccharide (LPS). In addition, several studies assessed enzymes involved in alcohol metabolism, specifically alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).

Figure 1

Figure 1. Flow diagram of study selection.

Table 1

Table 1. Basic characteristics of included studies.

Risk of bias assessment

In this analysis, most studies showed a low risk of bias for incomplete outcome data and selective reporting. Still, many had unclear or high risk regarding random sequence generation and blinding of participants or outcome assessors. Overall, the methodological quality varied, with some studies showing notable limitations in design and execution (Table 2). Overall, while the methodological rigor was acceptable in most trials, the notable sources of bias highlight the need for cautious interpretation of pooled results.

Table 2

Table 2. Quality of included studies in the meta-analysis.

Alcohol metabolism

Two studies evaluated the impact of probiotics on blood alcohol concentrations (ADH activity) and blood acetaldehyde levels (ALDH activity) in patients with alcoholic liver disease. The meta-analysis detected no significant pooled effects for either biomarker: blood alcohol (WMD = −2.08; 95% CI: −8.42 to 4.25; p = 0.520) or acetaldehyde (WMD = 2.52; 95% CI: −12.70 to 7.65; p = 0.627) (Figure 2). Heterogeneity was moderate for blood alcohol (I² = 60.9%) and low for acetaldehyde (I² = 37.3%). Although statistically non-significant, all included studies demonstrated a consistent reduction in these biomarkers following probiotic supplementation. The consistent reduction across studies suggests a potential metabolic effect of probiotics, warranting confirmation through larger, methodologically robust clinical trials.

Figure 2

Figure 2. The effects of probiotic supplementation on ADH, and ALDH.

Liver function parameters

The meta-analysis of 11 comparisons revealed that probiotic supplementation significantly reduced ALT (WMD = −10.10; 95% CI: −15.34, −4.87; p < 0.001), with moderate heterogeneity (I² = 66.8%; p < 0.001) (Figure 3). Probiotics supplementation significantly reduced AST (10 studies), with a pooled WMD of −13.05 (95% CI: −21.33, −4.78; p < 0.001) and substantial heterogeneity (I² = 82.3%, p < 0.001) (Figure 4). Also, probiotics did not have a significant effect on GGT (WMD = −13.73; 95% CI: −31.48, 4.02; p = 0.130; I² = 80.3%, p < 0.001) (Figure 5), and ALP (WMD = 3.35; 95% CI: −6.43, 13.14; p = 0.501; I² = 38.3%, p = 0.198) (Figure 6).

Figure 3

Figure 3. The effects of probiotic supplementation on ALT.

Figure 4

Figure 4. The effects of probiotic supplementation on AST.

Figure 5

Figure 5. The effects of probiotic supplementation on GGT.

Figure 6

Figure 6. The effects of probiotic supplementation on ALP.

Sensitivity analysis confirmed the robustness of our findings on ALT and AST (p < 0.05). Sensitivity analysis showed that excluding the Jung et al. study (21) substantially changed the estimated effect of probiotics on GGT (WMD = −21.14; 95% CI: −37.23, −5.05; p < 0.05). Begg’s and Egger’s tests did not indicate bias due to small study effects (p > 0.05). Asymmetry was observed in the funnel plot, possibly due to publication bias for GGT (Supplementary Figures 1–3). However, the trim-and-fill analysis yields a similar result to the overall result (WMD = −16.74; 95% CI: −34.05, 0.55; p ˃ 0.05) (Supplementary Figure 4).

Inflammatory biomarkers

Our finding revealed that probiotics had no considerable impact on LPS (WMD = −0.30; 95% CI: −0.86, 0.26; p = 0.720; I² = 0.0%, p = 0.443), TNF-a (WMD = 0.74; 95% CI: −8.83, 10.31; p = 0.182; I² = 94.5%, p < 0.001), IL-1B (WMD = 9.45; 95% CI: −20.66, 39.57; p = 0.406; I² = 86.9%, p < 0.001), and IL-6 (WMD = −5.30; 95% CI: −16.04, 5.44; p = 0.428; I² = 83.8%, p = 0.002) (Figure 7). The meta-analysis showed that probiotic supplementation did not lead to a statistically significant increase in IL-10 levels compared with the control group (WMD = 43.40; 95% CI: −29.62 to 116.42; p = 0.242; I² = 99.6%, p < 0.001) (Figure 7).

Figure 7

Figure 7. The effects of probiotic supplementation on LPS, TNF-a, IL-, IL-10 and IL-6.

Microbial analysis

Clinical studies (Table 3) show that probiotic supplementation in ALD enriches beneficial bacteria (Lactobacillus, Bifidobacterium, Faecalibacterium, Prevotella, Roseburia) and reduces potentially pathogenic taxa (Escherichia, Shigella, Klebsiella, Enterococci, Proteobacteria, Fusobacteria), improves gut microbial balance, and may affect both alpha and beta diversity, suggesting potential therapeutic benefits.

Table 3

Table 3. Changes in intestinal flora after probiotic supplementation.

Discussion

Our systematic review and meta-analysis of 12 studies demonstrates that probiotic supplementation offers measurable benefits in ALD. The most robust finding was a significant reduction in hepatic transaminases: pooled weighted mean differences showed probiotics lowered ALT and AST by clinically meaningful margins (30). In contrast, effects on other liver enzymes (GGT) and (ALP) were not statistically significant in the primary analysis (although sensitivity testing suggested a possible GGT reduction after omitting one outlying trial). No significant pooled effects were detected for blood alcohol or acetaldehyde levels (ADH/ALDH activity), LPS, or the pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and anti-inflammatory cytokine IL-10. Microbial analyses from the included studies consistently showed enrichment of beneficial taxa (Lactobacillus, Bifidobacterium, Faecalibacterium, etc.) and reductions in pathogenic proteobacteria (Escherichia, Shigella, Klebsiella, Enterococcus, etc.) (30, 31).

These outcomes largely agree with previous reports. For example, Xiong et al. (30) found that probiotics significantly improved liver enzymes (ALT, AST, GGT) and serum albumin, while also increasing Bifidobacteria and reducing E. coli in ALD patients. Our ALT/AST findings mirror theirs, and like them, we saw no significant change in TNF-α or IL-6 (30). The consistency of enzyme improvement across studies strengthens confidence that probiotics have a genuine hepatoprotective effect. Mechanistically, these effects likely stem from modulation of the gut–liver axis: probiotics can restore intestinal barrier function, reduce endotoxin (LPS) leakage, and dampen TLR4-mediated hepatic inflammation (31, 32). For example, Lactobacillus species like LGG have demonstrated the ability to repair alcohol-induced intestinal damage and reduce oxidative stress in the liver (33). Probiotics strengthen tight junctions and increase mucus production, which reduces the translocation of pathogen-associated molecular patterns (PAMPs) and helps prevent excessive activation of the innate immune system in the liver.

Probiotics enhance the gut–liver axis by restoring barrier integrity and diminishing the translocation of microbial products (34). Chronic alcohol consumption damages the intestinal lining, enabling LPS and other toxins to reach the liver and promote inflammation (35). Probiotic supplementation re-establishes tight junctions, boosts SCFA production, and reduces gut permeability (36, 37). As a result, fewer endotoxins reach the portal circulation, potentially reducing TLR4-driven cytokine cascades in hepatocytes and Kupffer cells (38). This mechanism plausibly explains the lowered ALT/AST we observed (31).

Despite these improvements in enzyme activity, it was unexpected that systemic inflammatory markers remained unchanged or even decreased. Preclinical studies suggest probiotics should lower TNF-α and IL-6 (31), but our analysis did not find this. One possibility is that circulating cytokine levels do not fully capture local hepatic immune responses. Additionally, the trials varied widely in patient severity, intervention duration, and analytical methods, which may have diluted any signal.

The meta-analysis indicated that probiotic supplementation did not produce a statistically significant increase in IL-10 levels relative to the control group. This finding is somewhat unexpected given that in vitro studies consistently show that Bifidobacterium and Lactobacillus strains can induce IL-10 secretion (39). A plausible explanation is that IL-10 may already be upregulated in ALD as part of a compensatory anti-inflammatory mechanism, thereby limiting the observable incremental effect of probiotics. Additionally, heterogeneity in assay timing, measurement techniques, or probiotic strain composition across studies may have contributed to the absence of a detectable change. Collectively, these considerations highlight the need for larger, rigorously standardized clinical trials to more accurately characterize the immunomodulatory influence of probiotic therapy.

It is important to note that several outcomes, including blood alcohol concentrations, LPS levels, and pro-inflammatory cytokines such as TNF-α and IL-6, did not show statistically significant improvements with probiotic supplementation. These nonsignificant findings suggest that the therapeutic effects of probiotics in ALD are probably selective rather than widespread. Although our findings indicate a clear improvement in hepatic transaminases and gut microbial composition, the lack of significant changes in systemic inflammatory markers highlights the importance of cautious interpretation regarding the broader therapeutic benefits of probiotics. Variability in disease severity, probiotic strains, intervention durations, and analytic methods may have limited the ability to detect modest biological effects. Therefore, the current evidence suggests that probiotics may offer adjunctive, rather than comprehensive, benefits in ALD, and further standardized, well-powered trials are required to more precisely define their clinical impact.

Our review also emphasized consistent alterations in gut microbiota caused by probiotics. Although a formal meta-analysis of taxa was not possible, all trials showed an increase in beneficial genera and a decrease in pathogens following treatment. For example, several studies observed an increase in Bifidobacterium and a decrease in Escherichia levels with probiotic use (40). These microbial shifts likely play a role in the clinical effects: higher levels of SCFA-producing bacteria (such as Roseburia and Faecalibacterium) may enhance the gut barrier and reduce liver inflammation. This is consistent with other research indicating that probiotics can restore alcohol-related dysbiosis and prevent LPS leakage (41, 42). Although our quantitative results focused on biochemical markers, the consistent microbiome findings strengthen the conclusion that probiotics help restore gut–liver homeostasis in ALD.

Several limitations should be considered carefully. The trials included in the analysis were diverse in their design: they differed in probiotic strains (single or multi-species), doses, and treatment durations, which ranged from 1 to 8 weeks. Most patient populations consisted of adults with mild to moderate ALD, often from Asia, which may limit how applicable the findings are. Numerous studies were limited in size, and several exhibited unclear or substantial risk of bias concerning randomization and blinding procedures. This heterogeneity contributed to elevated I² statistics for certain outcomes (AST, TNF-α). Publication bias may exist, as indicated by asymmetry in the funnel plot for GGT, although the trim-and-fill analysis did not significantly alter the conclusion. All outcomes were surrogate biomarkers; no trial reported concrete clinical endpoints like progression to cirrhosis, mortality, or liver histology. Therefore, our results should be considered hypothesis-generating rather than conclusive evidence of clinical benefit.

Looking forward, future studies should standardize probiotic interventions by selecting strains with established gut-barrier or anti-inflammatory benefits and include longer follow-up periods to evaluate long-term effects. Using probiotics together with prebiotics or dietary changes could potentially increase their effectiveness. It will also be helpful to link microbial and metabolomic changes to clinical outcomes. Our meta-analysis offers the most thorough evidence to date that probiotics can help correct liver enzyme irregularities and restore gut balance in ALD. These findings suggest that probiotic therapy could be a useful supplement alongside abstinence and nutritional support. However, more extensive, carefully designed trials are necessary to truly determine its effect on outcomes that matter to patients.

Given the encouraging hepatoprotective signals, research priorities should include: (1) large-scale RCTs focusing on clinically relevant endpoints (liver histology, hospitalization, survival); (2) mechanistic studies in humans to link specific microbial shifts with biochemical improvements; and (3) exploration of personalized probiotics based on individual microbiome profiles. Integrating these approaches will clarify how best to harness the gut–liver axis in treating ALD.

Conclusion

Probiotic supplementation shows beneficial effects in patients with alcoholic liver disease. It significantly improves liver enzyme profiles, particularly ALT and AST. Probiotics also enhance gut microbiota by increasing beneficial bacteria and reducing pathogenic taxa. Effects on alcohol metabolism and inflammatory markers were inconsistent across studies. Variations in study design, probiotic strains, and intervention duration may explain these discrepancies. Future large-scale, high-quality trials are needed to confirm these therapeutic benefits and their clinical relevance.

Data availability statement

The original contributions presented in the study are included in the article/Supplementary material, further inquiries can be directed to the corresponding author.

Author contributions

MSaa: Investigation, Methodology, Project administration, Writing – original draft. ZS: Investigation, Methodology, Project administration, Software, Supervision, Validation, Writing – original draft, Writing – review & editing. MSal: Methodology, Project administration, Resources, Software, Writing – original draft. VA: Formal analysis, Investigation, Resources, Writing – original draft, Writing – review & editing. MR: Conceptualization, Funding acquisition, Methodology, Validation, Writing – original draft. AS: Funding acquisition, Methodology, Project administration, Resources, Writing – original draft, Writing – review & editing. BJ: Conceptualization, Funding acquisition, Methodology, Project administration, Writing – original draft, Writing – review & editing. ZA: Formal analysis, Methodology, Project administration, Resources, Writing – original draft, Writing – review & editing. WM: Investigation, Methodology, Project administration, Validation, Visualization, Writing – original draft, Writing – review & editing. MA: Formal analysis, Investigation, Methodology, Resources, Supervision, Validation, Writing – original draft, Writing – review & editing. MJ: Investigation, Methodology, Supervision, Validation, Writing – original draft, Writing – review & editing. AK: Investigation, Methodology, Supervision, Writing – original draft, Writing – review & editing.

Funding

The author(s) declared that financial support was received for this work and/or its publication. The Authors are grateful to the Researchers Supporting Project (ANUI2024M111), Alnoor University, Mosul, Iraq.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Generative AI statement

The author(s) declared that Generative AI was used in the creation of this manuscript. We acknowledge the use of ChatGPT (GPT-4, OpenAI’s large-scale language-generation model) for assistance in editing and improving the writing style of this article. The AI was used solely for language enhancement and not for creating the content or references of the manuscript. The authors carefully reviewed, edited, and revised all AI-assisted texts and take full responsibility for the content and accuracy of this article.

Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Supplementary material

The Supplementary material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fnut.2025.1717393/full#supplementary-material

References

1. Sohi, I, Franklin, A, Chrystoja, B, Wettlaufer, A, Rehm, J, and Shield, K. The global impact of alcohol consumption on premature mortality and health in 2016. Nutrients. (2021) 13:3145. doi: 10.3390/nu13093145,

PubMed Abstract | Crossref Full Text | Google Scholar

2. Esser, MB, Leung, G, Sherk, A, Bohm, MK, Liu, Y, Lu, H, et al. Estimated deaths attributable to excessive alcohol use among US adults aged 20 to 64 years, 2015 to 2019. JAMA Netw Open. (2022) 5:e2239485–5. doi: 10.1001/jamanetworkopen.2022.39485,

PubMed Abstract | Crossref Full Text | Google Scholar

3. Xiao, J, Wang, F, Wong, NK, Lv, Y, Liu, Y, Zhong, J, et al. Epidemiological realities of alcoholic liver disease: global burden, research trends, and therapeutic promise. Gene Expr. (2020) 20:105–18. doi: 10.3727/105221620X15952664091823,

PubMed Abstract | Crossref Full Text | Google Scholar

4. Simpura, J. Trends in alcohol consumption and drinking patterns: sociological and economic explanations and alcohol policies. Nordic Stud Alcohol Drugs. (2001) 18:3–13. doi: 10.1177/145507250101801S07

Crossref Full Text | Google Scholar

5. Mak, KM, and Shekhar, AC. Lipopolysaccharide, arbiter of the gut–liver axis, modulates hepatic cell pathophysiology in alcoholism. Anat Rec. (2025) 308:975–1004. doi: 10.1002/ar.25562,

PubMed Abstract | Crossref Full Text | Google Scholar

6. Sosnowski, K, and Przybyłkowski, A. Ethanol-induced changes to the gut microbiome compromise the intestinal homeostasis: a review. Gut Microbes. (2024) 16:2393272. doi: 10.1080/19490976.2024.2393272,

PubMed Abstract | Crossref Full Text | Google Scholar

7. Szabo, G. Gut–liver axis in alcoholic liver disease. Gastroenterology. (2015) 148:30–6. doi: 10.1053/j.gastro.2014.10.042,

PubMed Abstract | Crossref Full Text | Google Scholar

8. Wang, S-C, Chen, YC, Chen, SJ, Lee, CH, and Cheng, CM. Alcohol addiction, gut microbiota, and alcoholism treatment: a review. Int J Mol Sci. (2020) 21:6413. doi: 10.3390/ijms21176413,

PubMed Abstract | Crossref Full Text | Google Scholar

9. Hyun, JY, Kim, SK, Yoon, SJ, Lee, SB, Jeong, JJ, Gupta, H, et al. Microbiome-based metabolic therapeutic approaches in alcoholic liver disease. Int J Mol Sci. (2022) 23:8749. doi: 10.3390/ijms23158749,

PubMed Abstract | Crossref Full Text | Google Scholar

10. Zhang, J, Li, C, Duan, M, Qu, Z, Wang, Y, Dong, Y, et al. The improvement effects of weizmannia coagulans BC99 on liver function and gut microbiota of long-term alcohol drinkers: a randomized double-blind clinical trial. Nutrients. (2025) 17:320. doi: 10.3390/nu17020320,

PubMed Abstract | Crossref Full Text | Google Scholar

11. Sun, H, Park, S, Mok, J, Seo, J, Lee, ND, and Yoo, B. Efficacy and safety of Wilac L probiotic complex isolated from kimchi on the regulation of alcohol and acetaldehyde metabolism in humans. Foods. (2024) 13:3285. doi: 10.3390/foods13203285,

PubMed Abstract | Crossref Full Text | Google Scholar

12. Kirpich, IA, Solovieva, NV, Leikhter, SN, Shidakova, NA, Lebedeva, OV, Sidorov, PI, et al. Probiotics restore bowel flora and improve liver enzymes in human alcohol-induced liver injury: a pilot study. Alcohol. (2008) 42:675–82. doi: 10.1016/j.alcohol.2008.08.006,

PubMed Abstract | Crossref Full Text | Google Scholar

13. Mishra, G, Singh, P, Molla, M, Yimer, YS, Dinda, SC, Chandra, P, et al. Harnessing the potential of probiotics in the treatment of alcoholic liver disorders. Front Pharmacol. (2023) 14:1212742. doi: 10.3389/fphar.2023.1212742,

PubMed Abstract | Crossref Full Text | Google Scholar

14. Xu, S, Zhao, M, Wang, Q, Xu, Z, Pan, B, Xue, Y, et al. Effectiveness of probiotics and prebiotics against acute liver injury: a meta-analysis. Front Med. (2021) 8:739337. doi: 10.3389/fmed.2021.739337,

PubMed Abstract | Crossref Full Text | Google Scholar

15. Faghfouri, AH, Afrakoti, LGMP, Kavyani, Z, Nogourani, ZS, Musazadeh, V, Jafarlou, M, et al. The role of probiotic supplementation in inflammatory biomarkers in adults: an umbrella meta-analysis of randomized controlled trials. Inflammopharmacology. (2023) 31:2253–68. doi: 10.1007/s10787-023-01332-8,

PubMed Abstract | Crossref Full Text | Google Scholar

16. Moher, D, et al. Preferred reporting items for systematic review and meta-analysis protocols (PRISMA-P) 2015 statement. Syst Rev. (2015) 4:1. doi: 10.1186/2046-4053-4-1,

PubMed Abstract | Crossref Full Text | Google Scholar

17. Armijo-Olivo, S, Stiles, CR, Hagen, NA, Biondo, PD, and Cummings, GG. Assessment of study quality for systematic reviews: a comparison of the Cochrane collaboration risk of Bias tool and the effective public health practice project quality assessment tool: methodological research. J Eval Clin Pract. (2012) 18:12–8. doi: 10.1111/j.1365-2753.2010.01516.x,

PubMed Abstract | Crossref Full Text | Google Scholar

18. Sánchez-Meca, J, and Marín-Martínez, F. Confidence intervals for the overall effect size in random-effects meta-analysis. Psychol Methods. (2008) 13:31–48. doi: 10.1037/1082-989X.13.1.31,

PubMed Abstract | Crossref Full Text | Google Scholar

19. Huedo-Medina, T.B., et al. <>Assessing heterogeneity in meta-analysis: Q statistic or I² index?</i> Psychol Methods, 2006. 11:193.

Google Scholar

20. Christopher Frey, H, and Patil, SR. Identification and review of sensitivity analysis methods. Risk Anal. (2002) 22:553–78. doi: 10.1111/0272-4332.00039,

PubMed Abstract | Crossref Full Text | Google Scholar

21. Jung, S, et al. Regulation of alcohol and acetaldehyde metabolism by a mixture of lactobacillus and bifidobacterium species in human. Nutrients, vol. 13 (2021).

Google Scholar

22. Li, X, Liu, Y, Guo, X, Ma, Y, Zhang, H, and Liang, H. Effect of Lactobacillus casei on lipid metabolism and intestinal microflora in patients with alcoholic liver injury. Eur J Clin Nutr. (2021) 75:1227–36. doi: 10.1038/s41430-020-00852-8,

PubMed Abstract | Crossref Full Text | Google Scholar

23. Stadlbauer, V, Mookerjee, RP, Hodges, S, Wright, GAK, Davies, NA, and Jalan, R. Effect of probiotic treatment on deranged neutrophil function and cytokine responses in patients with compensated alcoholic cirrhosis. J Hepatol. (2008) 48:945–51. doi: 10.1016/j.jhep.2008.02.015,

PubMed Abstract | Crossref Full Text | Google Scholar

24. Zhang, D, Hao, X, Yang, T, and Lou, Y. The therapeutic role of liver combined Bifidobacterium, lactobacillus and enterococcus in alcoholic liver disease. China Med. (2011) 6:555–8.

Google Scholar

25. Koga, H, Tamiya, Y, Mitsuyama, K, Ishibashi, M, Matsumoto, S, Imaoka, A, et al. Probiotics promote rapid-turnover protein production by restoring gut flora in patients with alcoholic liver cirrhosis. Hepatol Int. (2013) 7:767–74. doi: 10.1007/s12072-012-9408-x,

PubMed Abstract | Crossref Full Text | Google Scholar

26. Han, SH, Suk, KT, Kim, DJ, Kim, MY, Baik, SK, Kim, YD, et al. Effects of probiotics (cultured Lactobacillus subtilis/Streptococcus faecium) in the treatment of alcoholic hepatitis: randomized-controlled multicenter study. Eur J Gastroenterol Hepatol. (2015) 27:1300–6. doi: 10.1097/MEG.0000000000000458,

PubMed Abstract | Crossref Full Text | Google Scholar

27. Hui, Zhu, and Sheng, Wu Jian, Influence of Clostridium Butyricum tablets combined with polyene Phosphatidyl choline on intestinal flora and inflammatory factors of patients with alcoholic liver disease. 2019.

Google Scholar

28. Gupta, H, Kim, SH, Kim, SK, Han, SH, Kwon, HC, and Suk, KT. Beneficial shifts in gut microbiota by Lacticaseibacillus rhamnosus R0011 and Lactobacillus helveticus R0052 in alcoholic hepatitis. Microorganisms. (2022) 10:1474. doi: 10.3390/microorganisms10071474,

PubMed Abstract | Crossref Full Text | Google Scholar

29. Vatsalya, V, Feng, W, Kong, M, Hu, H, Szabo, G, McCullough, A, et al. The beneficial effects of lactobacillus GG therapy on liver and drinking assessments in patients with moderate alcohol-associated hepatitis. Am J Gastroenterol. (2023) 118:1457–60. doi: 10.14309/ajg.0000000000002283,

PubMed Abstract | Crossref Full Text | Google Scholar

30. Xiong, S-Y, Wu, GS, Li, C, Ma, W, and Luo, HR. Clinical efficacy of probiotics in the treatment of alcoholic liver disease: a systematic review and meta-analysis. Front Cell Infect Microbiol. (2024) 14:1358063. doi: 10.3389/fcimb.2024.1358063,

PubMed Abstract | Crossref Full Text | Google Scholar

31. Vidya Bernhardt, G, Shivappa, P, J, RP, Ks, R, Ramakrishna Pillai, J, Kumar Srinivasamurthy, S, et al. Probiotics—role in alleviating the impact of alcohol liver disease and alcohol deaddiction: a systematic review. Front Nutr. (2024) 11:1372755. doi: 10.3389/fnut.2024.1372755,

PubMed Abstract | Crossref Full Text | Google Scholar

32. Ye, W, Chen, Z, He, Z, Gong, H, Zhang, J, Sun, J, et al. Lactobacillus plantarum-derived postbiotics ameliorate acute alcohol-induced liver injury by protecting cells from oxidative damage, improving lipid metabolism, and regulating intestinal microbiota. Nutrients. (2023) 15:845. doi: 10.3390/nu15040845,

PubMed Abstract | Crossref Full Text | Google Scholar

33. Forsyth, CB, Farhadi, A, Jakate, SM, Tang, Y, Shaikh, M, and Keshavarzian, A. Lactobacillus GG treatment ameliorates alcohol-induced intestinal oxidative stress, gut leakiness, and liver injury in a rat model of alcoholic steatohepatitis. Alcohol. (2009) 43:163–72. doi: 10.1016/j.alcohol.2008.12.009,

PubMed Abstract | Crossref Full Text | Google Scholar

34. Meng, X, Li, S, Li, Y, Gan, RY, and Li, HB. Gut microbiota’s relationship with liver disease and role in hepatoprotection by dietary natural products and probiotics. Nutrients. (2018) 10:1457. doi: 10.3390/nu10101457,

PubMed Abstract | Crossref Full Text | Google Scholar

35. Dukić, M, Radonjić, T, Jovanović, I, Zdravković, M, Todorović, Z, Kraišnik, N, et al. Alcohol, inflammation, and microbiota in alcoholic liver disease. Int J Mol Sci. (2023) 24:3735. doi: 10.3390/ijms24043735,

PubMed Abstract | Crossref Full Text | Google Scholar

36. Karimi, R., and Hosseinzadeh, D. Probiotics and gastro-intestinal disorders: Augmentation, enhancement, and strengthening of epithelial lining probiotics 2024 CRC Press 188–215

Google Scholar

37. Shini, S, and Bryden, W. Probiotics and gut health: linking gut homeostasis and poultry productivity. Anim Prod Sci. (2021) 62:1090–112. doi: 10.1071/AN20701,

PubMed Abstract | Crossref Full Text | Google Scholar

38. Henao-Mejia, J, Elinav, E, Thaiss, CA, Licona-Limon, P, and Flavell, RA. Role of the intestinal microbiome in liver disease. J Autoimmun. (2013) 46:66–73. doi: 10.1016/j.jaut.2013.07.001,

PubMed Abstract | Crossref Full Text | Google Scholar

39. Moreno, D, de Leblanc, A, et al. Importance of IL-10 modulation by probiotic microorganisms in gastrointestinal inflammatory diseases. ISRN Gastroenterol. (2011) 2011:892971. doi: 10.5402/2011/892971,

PubMed Abstract | Crossref Full Text | Google Scholar

40. Shu, Q, and Gill, HS. A dietary probiotic (Bifidobacterium lactis HN019) reduces the severity of Escherichia coli O157: H7 infection in mice. Med Microbiol Immunol. (2001) 189:147–52. doi: 10.1007/s430-001-8021-9,

PubMed Abstract | Crossref Full Text | Google Scholar

41. Pisarello, MJL, Marquez, A, Chaia, AP, and Babot, JDCentro de Referencia para Lactobacilos (CERELA)-CCT NOA Sur-CONICET, 4000, San Miguel de Tucumán, Tucumán, ArgentinaUniversidad Nacional de Tucumán, 4000, San Miguel de Tucumán, Tucumán, Argentina, et al. Targeting gut health: probiotics as promising therapeutics in alcohol-related liver disease management. AIMS microbiology. (2025) 11:410–35. doi: 10.3934/microbiol.2025019,

PubMed Abstract | Crossref Full Text | Google Scholar

42. Yang, F, Li, X, Sun, J, Pang, X, Sun, Q, and Lu, Y. Regulatory mechanisms of the probiotic-targeted gut-liver axis for the alleviation of alcohol-related liver disease: a review. Crit Rev Food Sci Nutr. (2025) 65:6963–84. doi: 10.1080/10408398.2025.2455954,

PubMed Abstract | Crossref Full Text | Google Scholar