Beta-2-agonists enhance host defense functions in airway mucosa
MedWire News: Long-acting beta-2-agonists exert host defense mechanisms in airway mucosa, US research shows.
As reported in the journal BMC Pulmonary Medicine, Hong Wei Chu (University of Colorado, Denver) and colleagues showed that human epithelial cells treated with albuterol and formoterol reduced the burden of the bacteria Mycoplasma pneumoniae.
The innate immune response in airway epithelial cells provides defense molecules that protect against respiratory burden, the group notes. One such protein, the host defense molecule short palate, lung, and nasal epithelial clone 1 (SPLUNC1), has been shown to have antimicrobial and anti-inflammatory properties.
As the extended use of exogenous antibiotics might cause drug resistance, making them less effective in eliminating infections common to chronic obstructive pulmonary disease (COPD), it would be beneficial to increase the airway production of endogenous antimicrobial substances to clear invading bacteria, say Chu and colleagues.
To investigate further, bronchial epithelial cells from eight healthy, eight asthmatic, and eight COPD individuals were grown in culture and treated with cigarette smoke extract (CSE) and/or interleukin (IL)-13. This was followed by M. pneumoniae infection and treatment with albuterol and formoterol for up to 7 days.
Treatment with albuterol and formoterol significantly decreased M. pneumonia levels in normal and asthma epithelial cells. Normal cells treated with M. pneumonia and albuterol showed an increase in SPLUNC1.
In contrast, COPD cells did not respond to drug treatment. Cells treated with IL-13 did not respond to drug treatment and had reduced production of SPLUNC1.
"We found that the drugs were capable of lowering the M. pneumonia burden, up to 40% reduction, of epithelial cells, and that they appeared to do so in part through the induction of SPLUNC1, especially in normal subjects," write Chu and colleagues.
The authors say that studies are needed to determine if adding a corticosteroid to beta-2-agonists can save the host defense functions of airway epithelial cells in COPD and in cells with IL-13 treatment.
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