KINETICS OF THE DEVELOPMENT AND RECOVERY OF THE LUNG FROM IGE-MEDIATED INFLAMMATION - DISSOCIATION OF PULMONARY EOSINOPHILIA, LUNG INJURY, AND EOSINOPHIL-ACTIVE CYTOKINES

Citation
Jr. Shaver et al., KINETICS OF THE DEVELOPMENT AND RECOVERY OF THE LUNG FROM IGE-MEDIATED INFLAMMATION - DISSOCIATION OF PULMONARY EOSINOPHILIA, LUNG INJURY, AND EOSINOPHIL-ACTIVE CYTOKINES, American journal of respiratory and critical care medicine, 155(2), 1997, pp. 442-448
Citations number
28
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
155
Issue
2
Year of publication
1997
Pages
442 - 448
Database
ISI
SICI code
1073-449X(1997)155:2<442:KOTDAR>2.0.ZU;2-M
Abstract
Events occurring up to 16 d after antigen challenge were characterized using a novel protocol employing four bronchoscopies, two segmental a ntigen challenge (SAG) procedures (on Days 1 and 2), and six bronchoal veolar lavages (BALs) (on Days 1, 2, 9, and 16) in three groups: ragwe ed allergic asthmatics with dual phase airway reactions (AA-D), allerg ic asthmatics with a single early airway reaction (AA-S), and nonaller gic nonasthmatic control subjects. In AA-D subjects, SAC produced a ma rked eosinophilic inflammatory response at 24 h associated with eosino phil degranulation (eosinophil cationic protein [ECP] in BAI. fluid) a nd lung injury, which largely resolved by Day 16. When the second anti gen-challenged segment (SAG performed on Day 2) was lavaged 7 d after challenge (Day 9), a persistent pulmonary eosinophilia was noted accom panied by universal elevations in ECP and albumin. Eosinophil-active c ytokines showed unique patterns: interleukin-5 (IL-5) increased in the antigen segment on Day 2 then returned to baseline after 7 d; granulo cyte-macrophage colony-stimulating factor (CM-CSF) peaked at Day 2 but was persistently elevated throughout Day 16 in antigen segments, and increased in control segments at late time points; IL-3 levels were co nstant and similar in antigen and control segments. Changes were speci fic to AA-D subjects in comparison with control subjects. Elements of the IgE-mediated pulmonary inflammatory response differ markedly in th eir development and resolution.