Wouldn’t it be nice to be able to prevent a cold altogether? Nowadays, people are attempting to do just that. They are trying to “boost” their immunity to prevent and fight colds. There are even several items on the market people are tempted to buy in order to do so. Items such as nutritional supplements, cold remedies and fortified foods claim to fight off colds by enhancing the immune system. However, according to a new study by the University of Michigan, this approach may actually be doing more harm than good.
The results of this study appeared online ahead of print in the journal PLoS Pathogens, which is currently available online. Marc B. Hershenson, M.D., professor of pediatrics and communicable diseases and director of the division of pediatric pulmonology, is the study’s senior author.
The study shows that in the airways, the immune response to the common cold is actually maladaptive. Mice engineered to have a reduced innate immune response to the common cold actually showed less – not more – airway inflammation and bronchoconstriction (airway spasm) following infection. These results may hold important implications for individuals with asthma who often experience life-threatening flare-ups due to infections with cold viruses.
“You often hear that people want to boost their immunity to prevent and fight colds,” says Hershenson. “However, boosting the immune response could increase inflammation. Up to now there have been no convincing data supporting the theory that the immune response might be deleterious. In our study, we offer the first direct evidence that limiting the immune response reduces the manifestations of rhinovirus infection.”
“In our model, cold-induced asthma flare-ups were caused by the body’s immune response to the virus, not the virus itself. Chemicals produced by the immune system inflame cells and tissues, causing asthma symptoms such as cough and wheeze,” Hershenson explained.
Hershenson and his group hypothesized that limiting the immune response to viral infection would actually reduce their symptoms. Using a rhinovirus 1B, a cold virus strain that replicates in mouse lungs, they infected mice deficient in MDA5 and TLR3 – two receptors that trigger the protective defenses of the immune system against viruses and other pathogens.
MDA5-deficient mice showed a delayed defensive response to the infection leading to a small increase in the level of virus in the lungs. Nevertheless, these mice showed less airway inflammation and bronchoconstriction following infection compared to wild-type mice. TLR3-deficient mice also showed diminished airway responses.
In addition, MDA5- and TLR3-null mice that were made asthmatic by exposure to allergen showed decreased airway inflammatory and contractile responses in response to rhinovirus infection compared to normal mice. These results suggest reducing the mouse’s innate immune system led to reduced inflammatory signaling pathways and reduced airways inflammation and hyper-responsiveness in the context of rhinovirus infection.
“This study shows that, once you have a cold, elements of the immune response actually make the symptoms worse,” Hershenson adds. “A better strategy might be to modulate the immune response in asthma patients with colds.”
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