# Cytokine Profiles of Bronchoalveolar Lavage in Patients with Interstitial Lung Diseases and Non-Allergic Asthma

## TL;DR

This study compares cytokine and cell profiles in lung fluid from patients with immune-related lung diseases to identify biomarkers that could help diagnose and treat these conditions.

## Contribution

The study identifies nine BAL cytokine biomarkers that distinguish hypersensitivity pneumonitis and sarcoidosis, with RANTES and IL-6 linked to fibrotic outcomes.

## Key findings

- Nine cytokines (including IL-6 and RANTES) significantly differ in BAL fluid between hypersensitivity pneumonitis and sarcoidosis patients.
- Interstitial and obstructive lung diseases show distinct cytokine and cellular profiles.
- RANTES and IL-6 are associated with fibrotic outcomes in these diseases.

## Abstract

Diagnosing and prognosing immune-mediated airway diseases, like hypersensitivity pneumonitis (HP) and sarcoidosis, is complicated due to their overlapping symptoms and the lack of definitive biomarkers. Hence, we wanted to compare bronchoalveolar lavage (BAL) cytokine and chemokine profiles from 92 patients with different immune-mediated and inflammatory airway diseases, namely, HP, sarcoidosis, non-allergic asthma, amiodarone lung, and EGPA. We also compared pulmonary function parameters, BAL’s cellularity, and lymphocyte immunophenotypes. We found significant differences across all measured lung functions (VC, VC%, FEV1, FEV1%, and Tiff%) and in the number of macrophages, lymphocytes, neutrophils, and eosinophils. Furthermore, we showed significant differences in CD4, CD8, and CD4/8 across all included ILDs and OLDs; however, no significant differences were found in CD3, CD19, NK, or NKT. We identified nine biomarkers (IL-1β, IL-6, IL-8, IL-13, VEGF, angiogenin, C4a, RANTES, and MCP-1) that significantly differ in the BAL of patients with HP and sarcoidosis and showed that RANTES and IL-6 are associated with fibrotic outcome. We have demonstrated that interstitial and obstructive lung diseases differ in cytokine and cellular lung imprint, which may, in the future, enable the determination of the disease subtype and thus the identification of targets for the treatment of individuals or subgroups within diseases.