Michael T. Borchers

TL;DR: Results demonstrate that MPO and EPO contribute to tyrosine nitration in vivo and the major reactive nitrogen species formed by leukocyte peroxidase-catalyzed oxidation of NO 2 − is the one-electron oxidation product, ⋅NO2; and speculate that the latter reaction generates a labile Fe-ONOO complex, which might exist at sites of inflammation.

TL;DR: CD4+ T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology and it is suggested that eOSinophil effector functions impinge directly on lung function.

TL;DR: It is suggested that degranulation of eosinophils recruited to the lung in this model does not occur at levels comparable to those observed in humans with asthma, and that EPO activities are inconsequential to the development of allergic pulmonary pathologies in the mouse.

TL;DR: The relationship between eosinophils and the development of Ag-induced pulmonary pathologies, including airway hyper-responsiveness, was investigated using mice deficient for the secondary granule component, major basic protein-1 (mMBP-1).

TL;DR: The ablation of virtually all pulmonary eosinophils in OVA-treated mice resulted in a significant decrease in mucus accumulation and abolished allergen-induced airway hyperresponsiveness, demonstrating a direct causative relationship between allergenic-mediated pulmonary pathologies and eos inophils.