Mitochondrial DNA Damage and Inflammatory Markers in Bronchoalveolar Lavage Fluid during Acute Exacerbations of...

This study aimed to characterize the alterations in mitochondrial DNA (mtDNA) damage and inflammatory markers in bronchoalveolar lavage fluid (BALF) from patients with bronchiectasis during acute exacerbations (AEs) and to investigate their potential contribution to airway inflammation and disease mechanisms.

A retrospective case-control study was conducted, enrolling 45 patients with AEs and 84 patients with stable bronchiectasis (stable control [SC] group). BALF samples were collected via bronchoscopy. mtDNA damage was assessed using quantitative PCR, and inflammatory markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), and interleukin-8 (IL-8), were quantified via enzyme-linked immunosorbent assay. Multivariate logistic regression was performed to identify independent predictors of AEs, and Spearman correlation analysis was used to evaluate the relationships between mtDNA damage and inflammatory markers.

The AE group exhibited significantly lower mtDNA copy numbers and higher mtDNA deletion rates compared to the SC group (p < 0.001). Inflammatory markers, including IL-6, TNF-α, CRP, and IL-8, were markedly elevated in the AE group (p < 0.001). Spearman correlation analysis demonstrated a significant negative correlation between mtDNA copy number and all inflammatory markers, while mtDNA deletion rate was positively associated with inflammatory markers (p < 0.001). Moreover, multivariate logistic regression identified mtDNA copy number (odds ratio [OR] = 0.289, p = 0.026) and IL-6 (OR = 2.182, p = 0.038) as independent predictors of AEs.

mtDNA damage and elevated inflammatory marker levels in BALF are closely associated with AEs of bronchiectasis. These findings highlight their potential as biomarkers and therapeutic targets for future clinical application. Further studies are warranted to validate these observations and explore their role in the clinical management of bronchiectasis.