title: [Eosinophil apoptosis and asthma].
abstract: Eosinophils play an important role in airway inflammation in asthma. Eosinophils are believed through the release of their mediators to develop the irreversible structural airway changes. Dysregulation of apoptosis can lead to pathological accumulation of eosinophils in bronchial tissue. Apoptosis (programmed cell death) leads to the characteristic morphologic changes including reduction of the cellular volume, blebbing of the membrane, condensation of the nuclear chromatin, DNA laddering, mitochondrial dysregulation and finally to apoptotic bodies. Apoptosis can be induced by oncogenes, specific ligands and some cytokines. On the other hand IL-5, IL-3 and GM-CSF (granulocyte-macrophage-colony stimulating factor) dramatically increase the life span of eosinophils. Glucocorticoids promote eosinophil apoptosis and totally reverse the delayed death cased by beta2-agonists.
authors.affiliation: Katedra i Klinika Alergologii i Chorób Wewnetrznych AM w Bydgoszczy.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Dziedziczko
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Pałgan
mesh_terms: D058666:Adrenergic beta-2 Receptor Agonists; D017209:Apoptosis / Q000187:drug effects*; D001249:Asthma / Q000378:metabolism / Q000503:physiopathology*; D004804:Eosinophils / Q000378:metabolism*; D005938:Glucocorticoids / Q000494:pharmacology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism*; D006801:Humans; D007377:Interleukin-3 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D018343:Receptors, Adrenergic, beta-2 / Q000627:therapeutic use
chemical_list: D058666:Adrenergic beta-2 Receptor Agonists; D005938:Glucocorticoids; D007377:Interleukin-3; D015848:Interleukin-5; D018343:Receptors, Adrenergic, beta-2; D016178:Granulocyte-Macrophage Colony-Stimulating Factor