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Researchers in the Nuffield Department of Medicine, supported by NIHR Oxford Biomedical Research Centre (BRC), have discovered a link between potentially pathogenic bacteria and airways inflammation in people with severe asthma.

Woman using asthma inhaler

The team used long-read genome sequencing on sputum and nasal lavage samples from people with asthma to study the airway microbiome.

Until now, the specific species in the airway microbiome have not been identified; neither have the relationships between these species and mucosal immune responses in neutrophilic asthma, a severe type of asthma caused by an accumulation of white blood cells in the lungs.

The study was led by Professor Timothy Hinks, Associate Professor at the Respiratory Medicine Unit and Senior Research Fellow at BRC. He explained: ‘We have used a fairly new genome sequencing technique, produced by Oxford Nanopore Technologies, which allowed us to identify the bacteria at individual species level, where older technologies were less precise. It has allowed us to achieve the best description to date of the microbiome in the lung in the world’s most common respiratory disease: asthma.’

The team found that the microbiome in healthy people and those with mild asthma had similar microbial diversity in their samples. But 23% of the microbiomes in people with severe asthma were dominated by one of three respiratory pathogens: haemophilus influenzae, moraxella catarrhalis or streptococcus pneumoniae.

Prof Timothy Hinks also said, ‘We found that these three pathogens – which in our group we call the three musketeers – manage to survive where very few other bacteria can. The lung is usually very efficient at clearing out bacteria, so each of these bugs has evolved ways of surviving and persisting in the human airways. By integrating the bacteria we found with markers of the immune response, we have acquired new insights into how these pathogens manage to evade the immune system.’

Early indications suggest that Haemophilus induces IL-10, an anti-inflammatory molecule, and this is perhaps helping it to evade immune detection.

Read the full paper in Allergy, the European Academy of Allergy and Clinical Immunology: https://onlinelibrary.wiley.com/doi/10.1111/all.16269

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