Spring brings breezes, wheezes, and pollen oxidases

Abstract

While the release of pollen into the air is essential for the reproduction of plants, the accidental yet inevitable uptake of pollen into human airways can cause symptoms of seasonal allergies and asthma. The symptomatic response to pollen is caused by granulocytes that produce inflammation, which is due in part to oxidative stress through the action of NADPH oxidases. The recruitment of these inflammatory granulocytes was previously thought to depend entirely on the activation of an adaptive immune response. In this issue of the JCI, Boldogh et al. demonstrate that pollens contain endogenous NADPH oxidase activity, which functions to generate local "danger signals" in nearby airway epithelium. These signals in turn trigger the early recruitment of granulocytes, even in the absence of the adaptive immune response. These findings suggest that inhibition of the pollen oxidase may provide a way to antagonize allergic inflammation at a very early step.

Figure 1

A binary model for pollen-induced inflammation. Pollen triggers an adaptive immune response through the process of antigen presentation by professional antigen-presenting cells. This response also triggers recruitment of granulocytes including eosinophils and results in inflammation, which is due in part to the production of ROS by the eosinophil NADPH oxidase. In this issue of the JCI, Boldogh and colleagues (9) demonstrate that pollen has its own NADPH oxidase activity (referred to here as pollen oxidase, POX) that induces local oxidative stress and IL-8 secretion and triggers early recruitment of eosinophils even in the total absence of an adaptive immune response.