Abstract
BackgroundThere is evidence that bacterial colonisation in chronic obstructive pulmonary disease (COPD) is associated with increased neutrophilic airway inflammation. This study tested the hypothesis that different bacterial phyla and species cause different inflammatory profiles in COPD patients.MethodsSputum was analysed by quantitative polymerase chain reaction (qPCR) to quantify bacterial load and 16S rRNA gene sequencing to identify taxonomic composition. Sputum differential cell counts (DCC) and blood DCC were obtained at baseline and 6 months. Patients were categorised into five groups based on bacterial load defined by genome copies/ml of ≥ 1 × 104, no colonisation and colonisation by Haemophilus influenzae (H. influenzae), Moraxella catarrhalis (M. catarrhalis), Streptococcus pneumoniae (S. pneumoniae), or > 1 potentially pathogenic microorganism (PPM).ResultsWe observed an increase in sputum neutrophil (%), blood neutrophil (%) and neutrophil–lymphocyte ratio (NLR) in patients colonised with H. influenzae (82.6, 67.1, and 3.29 respectively) compared to those without PPM colonisation at baseline (69.5, 63.51 and 2.56 respectively) (p < 0.05 for all analyses), with similar findings at 6 months. The bacterial load of H. influenzae and Haemophilus determined by qPCR and 16s rRNA gene sequencing respectively, and sputum neutrophil % were positively correlated between baseline and 6 months visits (p < 0.0001, 0.0150 and 0.0002 with r = 0.53, 0.33 and 0.44 respectively).ConclusionsThese results demonstrate a subgroup of COPD patients with persistent H. influenzae colonisation that is associated with increased airway and systemic neutrophilic airway inflammation, and less eosinophilic airway inflammation.
Highlights
There is evidence that bacterial colonisation in chronic obstructive pulmonary disease (COPD) is associated with increased neutrophilic airway inflammation
The presence of bacterial infection in COPD patients during the stable state is associated with increased airway neutrophil numbers [6, 7]. It appears that different bacterial phyla are associated with different profiles of airway inflammation in COPD patients; raised blood and sputum eosinophils are associated with increased presence of the
We evaluated the stability of the relationship between the microbiome and airway inflammation using repeated samples at 6 months, primarily focusing on bacterial load measured by quantitative polymerase chain reaction and sputum cell counts
Summary
There is evidence that bacterial colonisation in chronic obstructive pulmonary disease (COPD) is associated with increased neutrophilic airway inflammation. The presence of bacterial infection in COPD patients during the stable state (i.e. not during exacerbations) is associated with increased airway neutrophil numbers [6, 7]. It appears that different bacterial phyla are associated with different profiles of airway inflammation in COPD patients; raised blood and sputum eosinophils are associated with increased presence of the. A study of microbiome, transcriptome and proteome profiling showed that H. influenzae presence in the stable state was associated with a unique profile of inflammation, including increased sputum neutrophil counts [10, 11]. The mechanistic reasons for increased ICS effects at higher blood eosinophil counts may be related to an inflammatory profile associated with increased levels of T2 cytokines, but an association with a different microbiome profile may be important [10]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
