( Researchers from University of Texas Me...)New Insight Gained For Allergic Reactions,Health

Researchers from University of Texas Medical Branch at Galveston have found that there may be an additional factor that may cause the allergic reactions// and asthma other than the body’s immune system reacting to the allergens.

This factor is the damage caused by chemically hyperactive molecules known as “reactive oxygen species,” which are spawned by interactions between a single pollen-carried enzyme and the cells that line airways. And, the researchers say, if an effective way can be found to reduce that damage—called “oxidative stress”—new and powerful allergy and asthma therapies may result.

The research is published in the recent issue of the Journal of Clinical Investigation.

The researchers had worked for nearly four years conducting extensive test-tube and lab-mouse experiments to prove the paradigm shifting “two-signal concept” in detail. They zeroed in on a key enzyme known as NADPH oxidase, which they identified in grains of pollen produced by ragweed and 38 other plant pollens and molds linked to allergy and asthma attacks. Within minutes of exposure, ragweed pollen or its extract containing NADPH oxidase produces damaging reactive oxygen species in cell culture and, in experiments with mice, in their lungs and airway lining fluid. The resulting oxidative stress almost immediately prompted the production of inflammatory immune signaling molecules and accumulation of inflammatory cells, a downstream event common to lung and other type of allergic inflammations. By contrast, ragweed pollen extract from which NADPH oxidase had been removed produced no reactive oxygen species, and resulted in a much smaller increase in numbers of inflammatory immune cells.

The research shows that it takes both oxidative stress and antigenic exposure to get a robust allergy or asthma attack, and also that the first few minutes of the exposure is critical. These two signals play a vital role in inducing allergic inflammation. '"/>




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