BackgroundAsthma is a disease of chronic airway inflammation with heterogeneous features. Neutrophilic asthma is corticosteroid-insensitive asthma related to absence or suppression of TH2 process and increased TH1 and/or TH17 process. Macrolides are immunomodulatory drug that reduce airway inflammation, but their role in asthma is not fully known. The purpose of this study was to evaluate the role of macrolides in neutrophilic asthma and compare their effects with those of corticosteroids.MethodsC57BL/6 female mice were sensitized with ovalbumin (OVA) and lipopolysaccharides (LPS). Clarithromycin (CAM) and/or dexamethasone (DXM) were administered at days 14, 15, 21, 22, and 23. At day 24, the mice were sacrificed.ResultsAirway resistance in the OVA+LPS exposed mice was elevated but was more attenuated after treatment with CAM+DXM compared with the monotherapy group (p<0.05 and p<0.01). In bronchoalveolar lavage fluid study, total cells and neutrophil counts in OVA+LPS mice were elevated but decreased after CAM+DXM treatment. In hematoxylin and eosin stain, the CAM+DXM-treated group showed less inflammation additively than the monotherapy group. There was less total protein, interleukin 17 (IL-17), interferon γ, and tumor necrosis factor α in the CAM+DXM group than in the monotherapy group (p<0.001, p<0.05, and p<0.001). More histone deacetylase 2 (HDAC2) activity was recovered in the DXM and CAM+DXM challenged groups than in the control group (p<0.05).ConclusionDecreased IL-17 and recovered relative HDAC2 activity correlated with airway resistance and inflammation in a neutrophilic asthma mouse model. This result suggests macrolides as a potential corticosteroid-sparing agent in neutrophilic asthma.

Background: Although respiratory tract infection is one of the most important trigger factors for acute exacerbation of chronic obstructive pulmonary disease (AE-COPD), there are limited data on the epidemiologic patterns of microbiology in South Korea.Methods: A multicenter observational study was conducted in 28 hospitals in South Korea between January 2015 and December 2018. Adult COPD patients with moderate to severe acute exacerbations were eligible for the present study. They underwent all conventional tests to identify etiologic microbiologic pathogens. The primary outcome was the percentage of different microbiological pathogens that caused AE-COPD. Comparative microbiological analysis was performed between the patients with asthma-COPD overlap (ACO) and pure COPD. Results:We included 1,186 patients with AE-COPD. Pure COPD patients were 87.9% and ACO patients were 12.1%. Nearly half of the patients used an ICS-containing regimen and one-fifth used systemic corticosteroids. Among them, respiratory pathogens were found in 55.3%. Bacteria and viruses were found in 33% and 33.2%, respectively. Bacterial and viral coinfections were found in 10.9%. The most frequently detected bacteria were Pseudomonas aeruginosa (9.8%), and the most frequently detected virus was influenza A (10.4%). Multiple 7 bacterial infections were more likely found in ACO compared to pure COPD (8.3% vs 3.6%, p-value=0.016). Conclusion:Distinct microbiological patterns were identified in patients with moderate to severe AE-COPD in South Korea. These findings may improve evidence-based management for AE-COPD and become the basis for further research related with infectious pathogens in COPD patients.

Background: Evaluating the diaphragm muscle in chronic obstructive pulmonary disease (COPD) is important. However, the role of diaphragm ultrasound (DUS) in distinguishing the exacerbation status of COPD (AECOPD) is not fully understood. We set this study to evaluate the role of DUS as a biomarker for distinguishing the AECOPD. Methods: COPD patients who underwent DUS were enrolled between March 2020 and November 2020. The diaphragm thickening fraction (TF max ) and diaphragm excursion (DE max ) during maximal deep breathing were measured. Patients were divided into exacerbation and stable groups. Demographics, lung function, and DUS findings were compared between the two groups. Receiver operating characteristic curve and univariate/multivariate logistic regression analyses were performed. Results: Fifty-five patients were enrolled. The exacerbation group had a lower body mass index (BMI) (20.9 vs 24.2, p = 0.003), lower TF max (94.8 ± 8.2% vs 158.4 ± 83.5%, p = 0.010), and lower DE max (30.8 ± 11.1 mm vs 40.5 ± 12.5 mm, p = 0.007) compared to stable group. The areas under the TF max (0.745) and DE max (0.721) curves indicated fair results for distinguishing AECOPD. The patients were divided into low and high TF max and DE max groups based on calculated cut-off values. Low TF max (odds ratio [OR] 8.40; 95% confidence interval [CI] 1.55-45.56) and low DE max (OR 11.51; were associated with AECOPD after adjusting for age, sex, BMI, and lung functions. Conclusion: DUS showed the possibility of an imaging biomarker distinguishing AECOPD from stable status.