Asthma


 
Asthma  research at LRRI  is conducted by groups of investigators exploring both grant- and contract-driven investigations.  Investigators make full use of many of the unique capabilities available to them at LRRI,  such as state-of–the-art aerosol technologies,  and rodent and canine models of allergic disease.
 

 

Ted Barrett, PhD,  is an NIH- and FAMRI- (Flight Attendants Medical Research Institute) funded scientist interested in 1) the role of maternal allergic status on the allergic status of the offspring (canine and murine models); 2) the role of maternal and neonatal environmental exposures on lung viral infections and  the development and exacerbation of allergic asthma (canine and murine models); 3) the role of cigarette smoke and nicotine exposure on the response to pulmonary viruses and allergens (murine model).  In addition, Dr. Barrett has developed unique canine models of allergic asthma, rhinitis, and dermatitis that are highly utilized by pharmaceutical companies to test new treatment modalities.

 

Julie Wilder, Ph.D. is a NIH- and FAMRI-funded scientist interested in 1) the role of second-hand cigarette smoke in the development and manifestations of allergic asthma (murine model); 2) the genetic basis of strain-dependent disparate immune responses to pulmonary insults (murine model); and 3) the role of pulmonary dendritic cells in orchestrating pulmonary inflammation in response to both allergens and infectious agents (murine model).

 

Mohan Sopori, PhD, and his collaborators, who are funded by several sources including NIH and DOD, work on two research projects related to allergy and asthma.  The first delineates the mechanism by which nicotine modulates ragweed/house dust mite-induced lung inflammation, airway reactivity, mucous formation, and atopy in the Brown Norway rat model. The team is also determining the effects of nicotine on mast cell degranulation in a cell culture model.  In addition, Dr. Sopori’s group has previously reported that prenatal but not postnatal exposure of mice to cigarette smoke exacerbates an allergen-induced airway hyperresponsiveness. Currently they are evaluating the role of various muscarinic receptors and cAMP in the increase in airway resistance in this model. 

 

The scientists who participate in the Asthma Program at LRRI welcome collaborations with both academic and industry scientists.

 

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