University Of Bergen Study Detects Antibiotic Resistance Genes In Healthy Lower Airways And Identifies High Prevalence In Sarcoidosis Patients

Researchers at the University of Bergen find antibiotic resistance genes in 35% of healthy lungs and high levels in sarcoidosis patients despite low drug use.

By: AXL Media

Published: Mar 31, 2026, 11:22 AM EDT

Source: Information for this report was sourced from The University of Bergen

Mapping the Genetic Resistance of the Lower Airways

A groundbreaking study from the University of Bergen has provided a rare glimpse into the prevalence of antimicrobial resistance genes within the human respiratory system. Published in BMJ Open Respiratory Research, the study utilized bronchoscopy samples to analyze the microbiomes of patients with COPD, asthma, pulmonary fibrosis, and sarcoidosis. By employing shotgun metagenomics—a sequencing method that maps both the types of microbes present and their specific genetic properties—researchers were able to identify resistance markers in the lower airways, an area of the body previously understudied in this context.

Surprising Prevalence in Healthy Participants

One of the most significant findings of the research was the detection of resistance genes in 35% of the healthy control group. First author Guri Kringeland expressed surprise at this figure, as these individuals had no underlying lung pathology. This suggests that the lower respiratory tract may serve as a natural reservoir for antibiotic resistance genes, even in the absence of chronic illness. The discovery challenges the assumption that such genetic markers are only found in clinical settings or in individuals with a history of severe infections.

The Impact of Recent Antibiotic Consumption

As expected, the research confirmed that individuals who had recently used antibiotics carried a higher burden of resistance genes. This aligns with global medical consensus that the frequent use of antimicrobial drugs is a primary driver of resistance. Patients with pulmonary fibrosis showed a clearly higher prevalence of these genes, likely due to the repeated courses of treatment often required for the condition. However, the data highlights that even targeted clinical use can leave a lasting genetic footprint on the lung's microbial environment.