New research suggests a specific immune response to respiratory infection in babies greatly increases asthma risk as they grow up.
It has previously been established that children who suffered severe respiritory viral infections as babies are at increased risk of developing asthma. Now researchers from Washington University School of Medicine in St. Louis, United States, say they have discovered the mechanism behind this association.
After studying the effects of severe respiritory infections in mice they believe they have pinpointed a specific immune response which increases the chances of asthma developing. They say that it will be possible to block these immune effects to prevent the development of asthma.
According to Mitchell Grayson, M.D., assistant professor of medicine in the Division of Allergy and Immunology, and the study's lead author, one in five babies who have these severe respiritory viral infections go on to develop asthma, where as amongst those who don't only one in thirty develops the condition.
In their experiments Dr. Grayson and colleagues noticed that mice that developed asthma-like symptoms had an abnormal immune response following severe respiratory viral infection. These mice tended to produce antibodies and other immune chemicals more typical of an allergic response than a response to viral infection. This unusual immune response to infection paved the way for the development of asthma-like symptoms in the mice according to the research team. Their results are published in the latest edition of the Journal of Experimental Medicine.
The researchers believe that a similar mechanism is likely to account for the much higher prevalence of asthma in children who had severe respiritory viral infections when they were younger.
"We think genetically predisposed individuals will tend to have this kind of immune reaction to a severe respiratory viral infection," Dr. Grayson told the University's press office .
"In those people an allergic-type response could be part of their antiviral immune response. That sets them up to make antibodies against a lot of environmental substances, like pet dander or pollen, and they can go on to develop allergies or asthma."
The immune system has two distinct responses and which one is initiated depends on the nature of the foreign invader. The Th1 response is associated with infection, particularly viral infection, with the Th2 response being associated with a response to allergens and environmental substances. This research suggests that in some people there is more crossover than usual in these systems so that viral infection triggers the Th2 system as well as the Th1 which would be expected.
Asthma rates have been climbing steadily in industrialized nations for decades. It has been widely thought that this was down to increased population density and urbanization with a corresponding increase in exposure to pollution. Dr. Grayson believes this study suggests this is not the sole reason for the increase and that increased transmission of viral infections due to the increased population density may be a contributor.
Once Dr. Grayson and his team had identified the mechanism behind the development of asthma-like symptoms in the mice they went on to try interventions aimed at disrupting the process. They found that by altering the immune cells or removing the inflammatory chemicals they secreted they were able to prevent the overgrowth of the mucus-producing cells that contribute to the development of asthma.
Dr. Grayson believes that new approaches to asthma prevention are now possible: "This offers a different way of thinking about what happens in the development of asthma," he said. "It may be possible to prevent many cases of asthma and other chronic inflammatory airway diseases by stopping allergic-type antibody production after a severe viral infection in infants."
Source: Induction of high-affinity IgE receptor on lung dendritic cells during viral infection leads to mucous cell metaplasia. Journal of Experimental Medicine 2007 Oct 29;204(11):2759-69. Grayson MH, Cheung D, Rohlfing MM, Kitchens R, Spiegel DE, Tucker J, Battaile JT, Alevy Y, Yan L, Agapov E, Kim EY, Holtzman MJ.