Azithromycin during Acute Chronic Obstructive Pulmonary Disease Exacerbations Requiring Hospitalization (BACE). A Multicenter, Randomized, Double-Blind, Placebo-controlled Trial

Vermeersch, Kristina; Gabrovska, Maria; Aumann, Joseph; Demedts, Ingel K.; Corhay, J L; Marchand, Éric; Slabbynck, Hans; Haenebalcke, Christel; Haerens, Michiel; Hanon, Shane; Jordens, Paul; Peché, Rudi; Fremault, Antoine; Lauwerier, Tine; Delporte, Anja; Vandenberk, Bert; Willems, Rik; Everaerts, Stephanie; Belmans, Ann; Bogaerts, Kris; Verleden, Geert M.; Troosters, Thierry; Ninane, Vincent; Brusselle, Guy; Janssens, Wim

doi:10.1164/rccm.201901-0094oc

Cited by 58 publications

(52 citation statements)

References 36 publications

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“…28,29 The importance of this process is suggested by the link between the reduced phagocytic capacity of the AMs of patients with chronic obstructive pulmonary disease (COPD), and their failure to clear lung infections. 32 In mice, other phagocytic receptors, such as the macrophage receptor with collagenous structure (MARCO), are important for clearance of respiratory pathogens including Streptococcus pneumoniae and Mycobacterium tuberculosis. 32 In mice, other phagocytic receptors, such as the macrophage receptor with collagenous structure (MARCO), are important for clearance of respiratory pathogens including Streptococcus pneumoniae and Mycobacterium tuberculosis.…”

Section: Alveolar Macrophagesmentioning

confidence: 99%

“…30 This is associated with decreased expression of phagocytic molecules such as the mannose receptor, and may be restored by treatment with azithromycin, which increases the phagocytic capacity of AMs, 31 and may improve patient outcomes. 32 In mice, other phagocytic receptors, such as the macrophage receptor with collagenous structure (MARCO), are important for clearance of respiratory pathogens including Streptococcus pneumoniae and Mycobacterium tuberculosis. 33,34 In humans, MARCO polymorphisms that reduce phagocytic capacity in monocyte-derived macrophages are linked to tuberculosis susceptibility, 33 and lower MARCO expression on AMs from diabetic mice reduces their ability to phagocytose M. tuberculosis.…”

Section: Alveolar Macrophagesmentioning

confidence: 99%

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Tissue‐resident innate immunity in the lung

2019

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The lung is a unique organ that must protect against inhaled pathogens and toxins, without mounting a disproportionate response against harmless particulate matter and without compromising its vital function. Tissue-resident immune cells within the lung provide local immunity and protection from infection but are also responsible for causing disease when dysregulated. There is a growing appreciation of the importance of tissue-resident memory T cells to lung immunity, but non-recirculating, tissue-resident, innate immune cells also exist. These cells provide the first line of defence against pulmonary infection and are essential for co-ordinating the subsequent adaptive response. In this review, we discuss the main lung-resident innate immune subsets and their functions in common pulmonary diseases, such as influenza, bacterial pneumonia, asthma and inflammatory disorders.

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Section: Alveolar Macrophagesmentioning

confidence: 99%

Section: Alveolar Macrophagesmentioning

confidence: 99%

Tissue‐resident innate immunity in the lung

2019

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“…83e86 More recently, a study showed that azithromycin therapy also may have a role during the highest risk period after acute exacerbation of COPD (AECOPD). 87 In the study by Vermeersch and colleagues, 87 301 patients were enrolled after an AECOPD and received 3 months of azithromycin or placebo. 87 Patients that received therapy had a lower rate of treatment failure after 3 months compared with placebo (49 vs 60%, HR ¼ 0.73; 95%CI 0.53-1.01, P ¼ .0526).…”

Section: Macrolidesmentioning

confidence: 99%

Management of asthma COPD overlap

Maselli

Hanania

2019

Annals of Allergy, Asthma & Immunology

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Asthma-COPD Overlap (ACO) is not a distinct disease entity but a term applied to patients with clinical features of both asthma and COPD. Asthma-COPD Overlap is associated with greater morbidity than asthma and COPD alone and with relative treatment refractoriness, but information is sparse about its course and optimal treatment. Current treatment recommendations are based on consensus because most clinical studies in asthma and COPD have excluded patients with ACO. Initial management approach should include addressing environmental triggers as well as identifying and treating underlying comorbidities. In selecting pharmacologic therapies, patients with ACO should be treated early with an ICS and 1 or more long-acting bronchodilator. In patients with severe disease, every effort should be made to address and target the patient's treatable traits. A better understanding of the molecular mechanisms and drivers of airway inflammation in patients with ACO as well as the identification of novel biomarkers may lead to a more precise treatment approach for important unmet needs.

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“…Antibiotic use is considered to be one of the most important perturbations for the airway microbiota. In recent years, macrolides have been widely used in infectious diseases and a range of chronic in ammatory airway disorders, including cystic brosis, bronchiectasis, chronic obstructive pulmonary disease and persistent uncontrolled asthma [10][11][12][13][14]. Previous randomized placebo-controlled trials have shown that, after exposure to long-term macrolide therapy, a signi cant reduction in the diversity of respiratory microbiota and Haemophilus in uenzae load can be observed in patients with lung diseases [15,16].…”

Section: Introductionmentioning

confidence: 99%

Azithromycin exposure induces transient microbial composition shifts and decreases the airway microbiota resilience from PM2.5 stress in healthy adults: a randomized, double-blind, placebo-controlled trial

Du¹,

Zou²,

Deng³

et al. 2020

Preprint

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Background: Azithromycin, widely used in recent years, can change the airway microbiota in patients with chronic lung diseases. Little data exists regarding the effects of azithromycin administration on airway microbiota among healthy adults. Therefore, we conducted a randomized, double-blind, placebo-controlled trial to assess the process of variation and re-establishment of the airway microbiota after azithromycin exposure in healthy adults. Methods: Forty-eight healthy volunteers were enrolled and randomly assigned into two groups. 500mg azithromycin or placebo was administered once daily for 3 days. We collected the induced sputum at the day before the drugs administration (D0), the day after the treatment course was completed (D4), 14 days, 30 days and 60 days post-dosing. 16S rRNA gene sequencing and quantification were applied to the induced sputum samples. We collected the environmental information including air quality data [particulate matter (PM 2.5 ) and PM 10 , air quality index (AQI) values] that might have an influence on the airway microbiota during the study. The subjects’ respiratory tract infection (RTI) events during sampling were recorded. Results: Azithromycin didn’t alter bacterial load but significantly reduced species richness and Shannon index. Azithromycin exposure resulted in decrease in the detection rate and relative abundance of different families belonging to Veillonellaceae , Pasteurellaceae , Leptotrichiaceae , Neisseriaceae and Fusobacteriaceae . By contrast, the relative abundance of taxa belonging to Streptococcus increased immediately after azithromycin intervention. The shifts in the microbial community composition require about 14 days to recover while alpha-diversity recovered later. The high concentration of PM 2.5 contributed to a novel variability in microbial community composition of azithromycin group at D30 (30 days after baseline). The network analysis found that azithromycin altered the microbial interactions within airway microbiota. The influence was still obvious at D14 when the relative abundance of most taxa had returned to the baseline level. Conclusions: Azithromycin has transient effect in airway microbiota of healthy adults and decreases the ability of the airway microbiota resilient from PM 2.5 stress. The influence of azithromycin on microbial interactions is noteworthy though the airway microbiota has returned to the near-baseline level.Registration: Chinese Clinical Trial Registry (ChiCTR1800018494), September, 2018. http://www.chictr.org.cn/edit.aspx?pid=31269&htm=4

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Azithromycin during Acute Chronic Obstructive Pulmonary Disease Exacerbations Requiring Hospitalization (BACE). A Multicenter, Randomized, Double-Blind, Placebo-controlled Trial

Abstract: Augustinus-A Debrock (PI), P Ardies (Coordinator). Imelda ziekenhuis-T Lauwerier (PI), A Delbaere (Coordinator). UZ Brussel-W Vincken (PI), S Hanon (Co-I), D Schuermans, K Van Eeckhoudt (Coordinators). CHU St.-Pierre-V Ninane (PI), M Gabrovska (Co-I), F De Cock, S Carlier (Coordinators).

Cited by 58 publications

References 36 publications

Tissue‐resident innate immunity in the lung

Tissue‐resident innate immunity in the lung

Management of asthma COPD overlap

Azithromycin exposure induces transient microbial composition shifts and decreases the airway microbiota resilience from PM2.5 stress in healthy adults: a randomized, double-blind, placebo-controlled trial

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