Lower airways inflammatory response during rhinovirus colds

Area of Science:

• Immunology
• Respiratory Medicine
• Virology

Background:

• Human rhinovirus (HRV) is a primary cause of the common cold.
• The mechanisms linking viral infections to altered airway reactivity, particularly in asthma exacerbations, remain unclear.
• Changes in endobronchial cell populations are hypothesized to play a role.

Purpose of the Study:

• To investigate the association between experimental human rhinovirus infections and changes in airway reactivity.
• To examine the cellular infiltrate in the bronchial mucosa during HRV infection.
• To explore the potential link between these cellular changes and asthma exacerbations.

Main Methods:

• 17 adult volunteers, including 6 atopic asthmatics, underwent experimental HRV serotype 16 infection.
• Bronchial mucosal biopsies were collected before, during, and after infection.
• Immunohistochemical techniques were used to quantify mast cells, eosinophils, lymphocytes, and neutrophils.
• Histamine reactivity (PC20) was measured to assess airway responsiveness.

Main Results:

• A significant increase in histamine responsiveness (PC20) was observed during HRV infection (p = 0.048).
• Submucosal lymphocyte counts increased significantly (p = 0.05).
• Epithelial eosinophil counts significantly increased with infection (p = 0.042), persisting in asthmatics post-infection.

Conclusions:

• Rhinoviral common colds are associated with increased airway hyperresponsiveness.
• A lymphocytic and eosinophilic infiltrate in the bronchial mucosa accompanies HRV infection.
• These mucosal changes may contribute to altered airway responsiveness and asthma exacerbations.