Abstract:
Background. Acute lung injury (ALI) and acute respiratory
distress syndrome (ARDS) are acute respiratory failure
syndromes with a high mortality rate. Byproducts of alcohol
metabolism like acetaldehyde and reactive oxygen species
lead to oxidative stress and inflammation which could worsen
recovery outcomes, due to increased risks for conditions
like systemic inflammation, sepsis and immune dysfunction.
Objective of study. Investigate the mechanisms by
which alcohol use helps the development of ALI and ARDS.
Explore Wnt/β-catenin pathway as a therapeutic target to
counteract these effects. Material and methods. This article
is based on information gathered from publications and
literature published on PubMed, Google Scholar and NCBI.
Results. Patients with alcohol use disorder (AUD) have
a 2-4 times higher risk of developing ARDS. People with a
history of alcohol abuse have twice the risk of developing
sepsis and patients with sepsis are twice as likely to develop
ARDS. Alcohol is a major risk factor for the development of ALI/ARD as it increases the risk of aspiration and pulmonary
infection and disrupts the immune system and nonimmunologic
host defense mechanisms leading to immune
dysregulation of alveolar macrophages and dysfunction of
the alveolar epithelial barrier. Alcohol Use Disorder (AUD)
heightens ALI/ARDS risk by decreasing immune defenses
and lung barrier functions via affecting membrane permeability,
glutathione depletion and impairment of macrophage
function. Wnt/β-catenin pathway offers therapeutic
potential by suppressing epithelial mesenchymal transition
for reducing lung injury. Conclusion. Alcohol consumption
greatly increases the risk of ALI and ARDS by disrupting
immune defenses and weakening lung barriers, causing enhanced
inflammation and oxidative stress. Targeting mechanisms
like the Wnt/β-catenin pathway may offer therapeutic
benefits to counteract these effects.
