TUESDAY, March 27, 2012 (HealthDay News) -- The common cold appears to increase the number of "cough receptors" in the airways and makes them more sensitive, which triggers coughing, wheezing and breathlessness, a new study reports.
People with asthma are especially vulnerable to this virus-induced coughing, said the researchers from Queen's University Belfast. The cough receptors also are known as transient receptor potential (TRP) receptors.
"TRP receptors respond to chemical and physical stimuli in the environment, such as pollutants in the air, a change in air temperature and some of the toxic chemicals found in cigarette smoke," said Dr. Hani'ah Abdullah, one of the researchers. "Once activated, these receptors cause the individual to cough and wheeze."
The study's findings were slated for presentation Tuesday at the Society for General Microbiology's spring meeting in Dublin, Ireland.
"The increase in receptor numbers makes individuals more sensitive to environmental stimuli, making them more likely to suffer from prolonged bouts of coughing," Abdullah said in a society news release.
The researchers took airway cells from healthy people and others with mild asthma and infected them with rhinovirus, the cause of many common colds. They found the virus triggered an increase in the number of cough receptors in the airway cells, particularly among those with asthma.
The study authors said their findings could help scientists develop drugs to effectively treat viral-induced coughing in those with chronic lung diseases.
"It's feasible that therapies could be developed that block either the sensitivity of cough receptors or their increase in number," Abdullah said. "This would keep symptoms under control and ultimately improve the lives of asthmatics."
Research presented at medical meetings should be considered preliminary until published in a peer-reviewed medical journal.
The U.S. Centers for Disease Control and Prevention provides more information on the common cold.
SOURCE: Society for General Microbiology, news release, March 27, 2012
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