title: Defining a link with asthma in mice congenitally deficient in eosinophils.
abstract: Eosinophils are often dominant inflammatory cells present in the lungs of asthma patients. Nonetheless, the role of these leukocytes remains poorly understood. We have created a transgenic line of mice (PHIL) that are specifically devoid of eosinophils, but otherwise have a full complement of hematopoietically derived cells. Allergen challenge of PHIL mice demonstrated that eosinophils were required for pulmonary mucus accumulation and the airway hyperresponsiveness associated with asthma. The development of an eosinophil-less mouse now permits an unambiguous assessment of a number of human diseases that have been linked to this granulocyte, including allergic diseases, parasite infections, and tumorigenesis.
authors.affiliation: Division of Pulmonary Medicine, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA. jjlee@mayo.edu
authors.forename: James J
authors.initials: JJ
authors.lastname: Lee
authors.forename: Dawn
authors.initials: D
authors.lastname: Dimina
authors.forename: MiMi P
authors.initials: MP
authors.lastname: Macias
authors.forename: Sergei I
authors.initials: SI
authors.lastname: Ochkur
authors.forename: Michael P
authors.initials: MP
authors.lastname: McGarry
authors.forename: Katie R
authors.initials: KR
authors.lastname: O'Neill
authors.forename: Cheryl
authors.initials: C
authors.lastname: Protheroe
authors.forename: Ralph
authors.initials: R
authors.lastname: Pero
authors.forename: Thanh
authors.initials: T
authors.lastname: Nguyen
authors.forename: Stephania A
authors.initials: SA
authors.lastname: Cormier
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Lenkiewicz
authors.forename: Dana
authors.initials: D
authors.lastname: Colbert
authors.forename: Lisa
authors.initials: L
authors.lastname: Rinaldi
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Ackerman
authors.forename: Charles G
authors.initials: CG
authors.lastname: Irvin
authors.forename: Nancy A
authors.initials: NA
authors.lastname: Lee
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology*; D004167:Diphtheria Toxin / Q000235:genetics; D047209:Eosinophil Peroxidase; D004804:Eosinophils / Q000502:physiology*; D018390:Gene Targeting; D007958:Leukocyte Count; D008168:Lung / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D023421:Models, Animal; D009093:Mucus / Q000378:metabolism; D010047:Ovalbumin / Q000276:immunology; D010446:Peptide Fragments / Q000235:genetics; D010544:Peroxidases / Q000235:genetics; D012130:Respiratory Hypersensitivity / Q000276:immunology / Q000473:pathology
chemical_list: D000485:Allergens; D004167:Diphtheria Toxin; D010446:Peptide Fragments; C029795:diphtheria toxin fragment A; D010047:Ovalbumin; D047209:Eosinophil Peroxidase; D010544:Peroxidases