Allergic reactions are taxing. Runny noses, watery eyes are a nuisance, but this condition may become fatal very quickly if not controlled. A strong anaphylaxis reaction can be triggered by common allergens like peanuts, dust or pollutants in the air and can be manifest as skin rash, cardio-respiratory failure and shock, eventually resulting in death.
Normally, females are considered to be more prone to allergies, which may secondary to the fact that men tend to be underdiagnosed. Women tend to show more symptoms because according to the study, the major hormone present in women, estradiol, which is a kind of estrogen, increases the amount and expression of eNOS.
In a response to any allergen, the body mediates defense mechanisms, which involves activation of mast cells and production of enzymes which cause the local blood vessels to dilate and pool the blood in the skin. This reaction is commonly brought about by a substance known as the endothelial nitric oxide synthases (eNOS).
“More women than men are admitted to hospitals for anaphylaxis, and that tells you something is going on here. Too often these gender differences are not focused on. We need to be better associating diseases with gender,” explains the study author Dean Metcalfe who is also the chief of Laboratory of Allergic Diseases at the National Institute of Allergy and Infectious Diseases.
In their study, the researchers used mice and induced anaphylactic reactions in them using substances like histamine, immunoglobulin G and immunoglobulin E to meter the reaction in male and female mice separately. they assessed the mice through body temperature, mediators released during an acute anaphylaxis response and levels of these mediators.
To study the effects of estrogen and eNOS fully, the researchers blocked the two compounds separately and saw that blocking estrogen brought the levels of allergic response down to that of males while blockage of eNOS completely demolishes the differences.
“Our study defines a contribution of estrogen through its regulation of eNOS expression and nitric oxide production to vascular hyperpermeability and intensified anaphylactic responses in female mice, providing additional mechanistic insights into risk factors and possible implications for clinical management in the further exploration of human anaphylaxis,” said the research team.