Analysis of Antimicrobial Peptide Expression Under Acute and Chronic Alcohol Exposure: A Cross-Sectional Study and a Systematic Review of the Literature.

Rojas-Pirela M, Herrera-Flores C, Costa-Alba P, Salete-Granado D, Aguilar ML, Puertas-Miranda D, Cicuéndez B, Pérez-Nieto MÁ, Pérez-Albornoz C, Folgueira C, Mora A, Sabio G, Marcos M

International journal of molecular sciences20 Feb 2026

PMID41752164PMCIDPMC12940937DOI10.3390/ijms27042026PepBankPUB-41752164

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Summary

Alcohol exposure affects immune regulation and tissue homeostasis. Antimicrobial peptides (AMPs) are essential components of innate immunity, not only defending against pathogens but also modulating processes such as inflammation. However, their tissue-specific regulation in response to alcohol remains poorly characterized, particularly in humans after acute intoxication. We evaluated the expression of AMPs in the peripheral blood of patients with alcohol use disorder (AUD, n = 9), individuals with acute alcohol consumption (AAC, n = 9), and controls using quantitative polymerase chain reaction (qPCR). Additionally, we analyzed AMP expression in selected tissues of mice exposed to chronic ethanol feeding (National Institute on Alcohol Abuse and Alcoholism model for 5 days) and performed a systematic review of AMP regulation in alcohol-related disorders (2005-2025; n = 36 studies, reflecting a limited and heterogeneous body of available evidence). Human cathelicidin antimicrobial peptide (LL-37), lipopolysaccharide-binding protein (LBP), and bactericidal/permeability-increasing protein (BPI) were significantly upregulated in patients with AUD, whereas LL-37 and LBP were significantly upregulated in AAC. In the livers of ethanol-fed mice, LEP2, LCN2, and LBP levels were markedly increased, whereas LL-37 and LEP1 were downregulated. Duodenal tissue exhibited upregulation of DEFB1. In adipose tissue, DEFA2 was significantly increased in peripheral depots, whereas only LCN2 was upregulated in brain tissue. The systematic review demonstrated complex, heterogeneous, and organ-dependent AMP regulation and also highlighted the paucity of human data on AAC, a gap that our study partially addresses. Our results are consistent with the hypothesis that selected AMPs may serve as candidate markers of organ damage or microbial translocation and as possible therapeutic targets, a hypothesis that requires confirmation in larger, adequately powered studies.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

No result from this study comes from a test of the peptide.

Natural levels measured3

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

01HumanEndogenous levelObservational studyOther
In patients with alcohol use disorder, LL‑37 expression in peripheral blood was significantly higher than in controls.
In plain wordsIn patients with alcohol use disorder, the body's own LL‑37 gene activity in blood was higher than in controls.
Peptide
LL-37
Outcome
IncreaseLL-37 expression in peripheral blood, alcohol use disorder
Study
n: not reported in source
Comparator
Controls
Outcome group
Immune response · Immune and inflammation
Source sentences
Summary
Human cathelicidin antimicrobial peptide (LL-37), lipopolysaccharide-binding protein (LBP), and bactericidal/permeability-increasing protein (BPI) were significantly upregulated in patients with AUD
1 context sentence(design, population, supporting numbers)
Summary · context
We evaluated the expression of AMPs in the peripheral blood of patients with alcohol use disorder (AUD, n = 9), individuals with acute alcohol consumption (AAC, n = 9), and controls using quantitative polymerase chain reaction (qPCR).
This result measures the body's own LL-37. Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-4175216401
02HumanEndogenous levelObservational studyOther
In individuals with acute alcohol consumption, LL‑37 expression in peripheral blood was significantly higher than in controls.
In plain wordsIn people who drank alcohol acutely, the body's own LL‑37 gene activity in blood was higher than in controls.
Peptide
LL-37
Outcome
IncreaseLL-37 expression in peripheral blood, acute alcohol consumption
Study
n: not reported in source
Comparator
Controls
Outcome group
Immune response · Immune and inflammation
Source sentences
Summary
whereas LL-37 and LBP were significantly upregulated in AAC
1 context sentence(design, population, supporting numbers)
Summary · context
We evaluated the expression of AMPs in the peripheral blood of patients with alcohol use disorder (AUD, n = 9), individuals with acute alcohol consumption (AAC, n = 9), and controls using quantitative polymerase chain reaction (qPCR).
This result measures the body's own LL-37. Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-4175216402
03AnimalEndogenous levelAnimal study (in vivo)Other
In the livers of mice fed ethanol, LL‑37 expression was downregulated.
In plain wordsIn mice fed ethanol, the body's own LL‑37 gene activity in the liver was lower.
Peptide
LL-37
Outcome
DecreaseLL-37 expression in liver of ethanol-fed mice
Study
mousen: not reported in source
Chronic ethanol feeding (NIAAA model, 5 days)
Outcome group
Immune response · Immune and inflammation
Source sentences
Summary
In the livers of ethanol-fed mice, LEP2, LCN2, and LBP levels were markedly increased, whereas LL-37 and LEP1 were downregulated.
1 context sentence(design, population, supporting numbers)
Summary · context
Additionally, we analyzed AMP expression in selected tissues of mice exposed to chronic ethanol feeding (National Institute on Alcohol Abuse and Alcoholism model for 5 days) and performed a systematic review of AMP regulation in alcohol-related disorders (2005-2025; n = 36 studies, reflecting a limited and heterogeneous body of available evidence).
This result measures the body's own LL-37. Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-4175216403

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 3Current
9 Oct 2026, 18:17 UTC
Study results updated
Version 2
9 Oct 2026, 03:03 UTC
Study data updated · source update from Europe PMC
Version 1
9 Oct 2026, 02:56 UTC
First added · source update from Europe PMC

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