New Study Uncovers Mechanism Responsible For Seasonal Allergies

Researchers have discovered an important mechanism in the process of becoming allergic to pollen that is responsible for the development of allergic asthma and seasonal allergies, according to a new study.

When exposed to airborne allergens, the immune system releases neutrophils—a type of white blood cell—to combat the invading substance and create inflammation. Individuals who suffer from seasonal allergies and allergic asthma experience heightened responses to these allergens over the course of repeated exposures.

Is Sublingual Immunotherapy the Best Option for Seasonal Allergies?
Allergic Rhinitis and Asthma: Role of Environmental Determinants

In order to evaluate how neutrophils are involved in the regulation of allergic response and inflammation, researchers exposed mice to ragweed pollen. They observed that when exposed to the allergen, the mice’s immune systems released proteins called chemokines with the purpose of attracting neutrophils to the site of the reaction. Next, they exposed mice that were genetically altered to lack the ability to synthesize chemokines, and therefore did not experience the inflammation caused by neutrophils.

"These data suggest that when the body is forced to react to the presence of pollen in the airways, it recruits neutrophils that induce a state of continuous oxidative stress in the airways. This type of cellular stress from any cause can worsen allergic asthma," researchers wrote.

"We suggest that inhibiting recruitment of neutrophils by blocking chemokines may be a unique strategy for preventing pollen-induced allergic disorders," they concluded.

The full study was published in the American Journal of Respiratory Cell and Molecular Biology.

—Michael Potts


Hosoki K, Aguilera-Aguirre L, Brasier AR, et al. Pollen-induced innate recruitment of neutrophils facilitates induction of allergic sensitization and airway inflammation. Am J Respir Cell Mol Biol. June 2015. [epub ahead of print] DOI: 10.1165/rcmb.2015-0044OC.