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Azithromycin attenuates airway inflammation in a mouse model of viral bronchiolitis

Avraham Beigelman¹, Cassandra L Mikols, Sean P Gunsten

¹Division of Allergy, Immunology & Pulmonary Medicine, Department of Pediatrics, Washington University School of Medicine, St, Louis, MO; USA. beigelman_a@kids.wustl.edu

Respiratory Research

|July 2, 2010

Insights

Azithromycin treatment reduced airway inflammation in a mouse model of viral bronchiolitis. This macrolide antibiotic demonstrated anti-inflammatory effects, suggesting potential for treating acute viral infections and preventing long-term consequences like asthma.

Area of Science:

Pulmonology
Infectious Diseases
Pharmacology

Background:

Viral bronchiolitis is a primary cause of infant hospitalization.
It is linked to childhood asthma and elderly morbidity/mortality.
Current therapies do not effectively manage acute inflammation or prevent post-viral asthma.

Purpose of the Study:

To investigate azithromycin's efficacy in attenuating acute and chronic airway inflammation in a mouse model of paramyxoviral bronchiolitis.

Main Methods:

Mice were infected with parainfluenza type 1 (SeV) and treated with azithromycin or PBS.
Airway inflammation, immune cells, and inflammatory mediators were assessed in lung tissue and bronchoalveolar lavage (BAL) on days 8 and 21.

Main Results:

Azithromycin significantly reduced post-viral weight loss and leukocyte accumulation in lung and BAL, particularly neutrophils.
Inflammation reduction was independent of viral load.
Azithromycin attenuated BAL inflammatory mediators and promoted resolution of chronic inflammation.

Conclusions:

Azithromycin effectively reduced acute and chronic airway inflammation in a mouse model of viral bronchiolitis.
These anti-inflammatory effects are independent of antiviral activity.
Findings support clinical trials on macrolides for viral bronchiolitis and its sequelae.

Read full analysis

Abstract

Background:

Viral bronchiolitis is the leading cause of hospitalization in young infants. It is associated with the development of childhood asthma and contributes to morbidity and mortality in the elderly. Currently no therapies effectively attenuate inflammation during the acute viral infection, or prevent the risk of post-viral asthma. We hypothesized that early treatment of a paramyxoviral bronchiolitis with azithromycin would attenuate acute and chronic airway inflammation.

Methods:

Mice were inoculated with parainfluenza type 1, Sendai Virus (SeV), and treated daily with PBS or azithromycin for 7 days post-inoculation. On day 8 and 21 we assessed airway inflammation in lung tissue, and quantified immune cells and inflammatory mediators in bronchoalveolar lavage (BAL).

Results:

Compared to treatment with PBS, azithromycin significantly attenuated post-viral weight loss. During the peak of acute inflammation (day 8), azithromycin decreased total leukocyte accumulation in the lung tissue and BAL, with the largest fold-reduction in BAL neutrophils. This decreased inflammation was independent of changes in viral load. Azithromycin significantly attenuated the concentration of BAL inflammatory mediators and enhanced resolution of chronic airway inflammation evident by decreased BAL inflammatory mediators on day 21.

Conclusions:

In this mouse model of paramyxoviral bronchiolitis, azithromycin attenuated acute and chronic airway inflammation. These findings demonstrate anti-inflammatory effects of azithromycin that are not related to anti-viral activity. Our findings support the rationale for future prospective randomized clinical trials that will evaluate the effects of macrolides on acute viral bronchiolitis and their long-term consequences.

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