sing just one model, however, it’s difficult to determine the role of eosinophils versus that model’s own genetic strategy.”
So instead of a single model, Rothenberg, Fulkerson and their colleagues used three different ones. They studied one mouse model in which eosinophils don’t develop from bone marrow, as they should, and two models in which eosinophils remain in the blood stream instead of rallying into the lung tissue to protect against asthma.
They then looked at the characteristics that all three models had in common so they could attribute any alteration in their appearance (or phenotype) to eosinophils, and not to that particular model’s genetics.
In the absence of eosinophils, the researchers report, they found that allergen-induced mucous production dropped in all models, suggesting that “eosinophils play a big role in mucous production in response to an allergen challenge.”
The researchers also report that eosinophils alter the lungs’ “micro environment” by stimulating production of the signaling cytokines. Involved in triggering the body’s immune defense mechanism to take action against infection, cytokines are responsible for almost all the characteristics of asthma.
“If cytokines are produced in the lungs, you’ll end up with asthma,” says Fulkerson. “But we found in eosinophil-free models that the cytokines that together produce almost all the visible symptoms of asthma—known as IL (Interleukin) 4 and IL 13—were markedly reduced.
Having shown that eosinophils play an important part in mucous production and airway obstruction in asthma, the researchers’ next goal was to determine how they actually do that.
Examination of mouse lung tissue revealed increased genetic activity associated with the characteristics of asthma: mucous, airway obstruction and hyperactivity.
“We took two of these models and looked at changes in gene expression in the lunPage: 1 2 3 Related medicine news :1
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