Impact of Esophageal Dilation and Smoking on Bronchoalveolar Lavage Immune Profiles, Cellular Distribution, and Lipid-Laden Macrophage Index in Idiopathic Pulmonary Fibrosis

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with a poor prognosis. Esophageal dilation and hiatal hernia are common in IPF and may facilitate microaspiration, exacerbating inflammation. We investigated the relationship between radiological esophageal dilation, smoking status, and bronchoalveolar lavage (BAL) cellular and immunological profiles in IPF patients. Methods: This retrospective study included 71 IPF patients. Esophageal diameters were measured at four levels (L1–L4) via high-resolution computed tomography (HRCT). BAL fluid was analyzed for differential cell counts, the Lipid-Laden Macrophage Index (LLMI), and T-lymphocyte subsets (CD4+, CD8+) using flow cytometry. Results: Esophageal dilation (diameter >10 mm) was present in 52.1% of patients, and 36.6% had a hiatal hernia. A significant negative correlation was found between distal esophageal dilation (L4) and BAL CD4+ counts (r = −0.267, p = 0.024). Similarly, the mean maximum esophageal diameter negatively correlated with BAL CD4+ levels (r = −0.288, p = 0.015). Patients with hiatal hernia had significantly higher BAL neutrophil percentages than those without (20.0% ± 4.39% vs. 8.93% ± 2.0%, p = 0.047). Furthermore, smokers exhibited significantly lower BAL CD4+ levels than non-smokers (p = 0.042). No significant correlation was found between esophageal dilation and the LLMI (p > 0.05). Conclusions: Esophageal dilation is significantly associated with altered local immune profiles in IPF. The negative correlation between distal esophageal dilation and BAL CD4+ counts, plus the link between hiatal hernia and neutrophilic inflammation, suggests an interplay between esophageal dysfunction and the pulmonary immune microenvironment. Radiological assessment of esophageal dilation may serve as a non-invasive surrogate marker for identifying high-risk clinical phenotypes in IPF.