Published Paper Details:

ABSTRACT Background Lung cancer development is a complex process influenced by genetic, environmental, inflammatory, and immunological factors. Chronic allergic airway inflammation, characterized by increased Th2 immune responses, eosinophilic activity, and altered cytokine expression, may influence the lung microenvironment and contribute to cancer initiation. Recent evidence suggests that lung microbiome dysbiosis can modify immune surveillance, inflammatory pathways, and tumor-promoting mechanisms. Understanding the relationship between allergic airway inflammation, lung microbiota alterations, and immune crosstalk may help identify early biomarkers for lung cancer prevention and targeted therapy. Objective To assess the impact of allergic airway inflammation on lung cancer initiation and evaluate the association between lung microbiome alterations and immune response among selected participants. Methods A quantitative observational comparative study was conducted among 100 participants divided into two groups: 50 participants with allergic airway inflammation (asthma/allergic airway disease) and 50 healthy controls. Participants were selected using purposive sampling. Clinical history, inflammatory biomarkers, microbiome profiles, and immune response parameters were assessed. Airway inflammation was evaluated using serum IgE levels, eosinophil count, and inflammatory cytokines (IL-4, IL-5, IL-13). Lung microbiome composition was analyzed using 16S rRNA sequencing of respiratory samples. Immune activity was assessed through inflammatory markers and immune regulatory pathways. Data were analyzed using SPSS version 26.0. Descriptive statistics, chi-square test, independent t-test, and correlation analysis were applied. Results Among participants with allergic airway inflammation, significant changes in airway microbiome composition were observed compared with controls. Reduced microbial diversity and increased abundance of inflammatory-associated bacterial species were identified. Higher levels of Th2-associated cytokines were found among allergic participants. Participants with chronic allergic inflammation showed: o Increased eosinophilic airway activity o Higher IgE concentration o Altered microbiome diversity o Enhanced inflammatory signaling pathways Microbiome imbalance showed a significant positive association with inflammatory markers (p<0.05), suggesting that allergic inflammation may contribute to a tumor-supportive lung microenvironment. Conclusion The findings indicate that allergic airway inflammation may influence lung cancer initiation through alteration of microbiome-immune interactions. Persistent inflammatory responses and microbial dysbiosis may contribute to impaired immune surveillance and early carcinogenic changes. Targeting microbiome regulation and inflammatory pathways may provide future opportunities for lung cancer prevention and immunotherapy strategies.