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The following is a summary of “NTHi killing activity is reduced in COPD patients and is associated with a differential microbiome,” published in the January 2025 issue of Pulmonology by Gopalakrishnan et al. 

Chronic obstructive pulmonary disease (COPD) was characterized as a chronic lung disease with airway obstruction and inflammation, and while non-typeable Haemophilus influenzae (NTHi) lung infections were known to be common in COPD, contributing to exacerbations and lung function decline, the relationship between these infections and immune responses remained poorly understood.  

Researchers conducted a retrospective study to investigate the characterization of the respiratory microbiome and mycobiome in patients, examining microbial dynamics and host immune changes linked to NTHi killing activity.  

They enrolled participants with mild-to-moderate COPD, including frequent and infrequent exacerbators, along with healthy volunteers (HV). The microbial composition, proteomics, and NTHi killing activity were assessed using bronchoalveolar lavage fluid (BALF). Additionally, antigen-antibody titers for COPD pathogens in sera were measured with a multiplex assay.  

The results showed the Actinobacteria and Bacteroidetes were more abundant in the BALF of COPD and HV subjects, respectively. A significant difference in IgA titer response against NTHi antigens was found between COPD and HV. Furthermore, COPD subjects had significantly higher NTHi killing activity in BALF (OR = 5.64; 95% CI = 1.75–20.20; P = 0.001). Stratification of patients with COPD by NTHi killing activity revealed unique microbial and protein profiles, with Firmicutes, Actinobacteria, and haptoglobin enriched in those with higher killing activity.  

Investigators concluded that differences in host immune responses and NTHi-killing activity were associated with microbiome changes in mild-to-moderate COPD, suggesting a potential link between the respiratory microbiome and immune activity against NTHi in COPD pathogenesis, even at early stages of the disease. 

Source: respiratory-research.biomedcentral.com/articles/10.1186/s12931-025-03113-z