Parasitic infections as immunomodulatory modifiers of chronic obstructive pulmonary disease

BackgroundChronic obstructive pulmonary disease (COPD) is a heterogeneous inflammatory lung disorder in which bacterial and viral infections are established contributors to exacerbation, parasitic infection remains underexplored in COPD immunopathology.ObjectiveTo critically synthesize evidence that parasitic infections modify COPD immunopathology and to identify clinically relevant implications and research priorities.MethodsPubMed/MEDLINE, Embase, Scopus, and Web of Science were searched for publications from January 1985 to July 2026; Google Scholar and reference lists supplemented retrieval. Evidence was synthesized narratively and classified as direct COPD-specific clinical evidence, indirect human pulmonary evidence, animal-model evidence, or mechanistic evidence.ResultsInfections with helminths and protozoa may influence the pathophysiology of COPD by modulating the type 1 immune response through type 2 polarization, expansion of regulatory T cells, eosinophilia, systemic immune activation, and alterations to the microbiome. These mechanisms may influence inflammatory phenotypes and exacerbation susceptibility. Direct COPD-specific evidence is limited. Most support derives from pulmonary parasitic disease, observational studies, animal models, or mechanistic inference. Clinically, parasitic eosinophilia may confound COPD phenotyping, and occult Strongyloides stercoralis infection is particularly important when systemic corticosteroids are considered.ConclusionCurrent evidence supports a biologically possible role for parasitic infections as modifiers of COPD immunopathology, but does not establish causality or routine parasite-driven COPD. Prospective, phenotype-stratified studies integrating parasitological and immunological analyses are required, particularly in endemic populations.