title: Acute allergic responses induce a prompt luminal entry of airway tissue eosinophils.
abstract: Traditionally, traffic and activation of eosinophils in asthmatic airways are thought to take place during the late-phase allergic reaction. The present study tests the hypothesis that when eosinophils are present in the tissue before allergen exposure, as in chronically inflamed asthmatic airways, acute anaphylactic reactions initiate an eosinophil response. Using a guinea-pig allergic model, where eosinophilia is present at baseline conditions, the traffic of resident eosinophils was examined in vivo immediately after allergen challenge. By 2 min after challenge, eosinophils had moved up to apical epithelial positions. Within 10 min, a marked migration of eosinophils into the airway lumen was demonstrated. Along with the allergen-induced egression of eosinophils, acute luminal entry of plasma proteins and eotaxin occurred. Eosinophil egression was effectively inhibited by the antiexudative drug formoterol, whereas the proexudative drug bradykinin could in naive animals evoke a prompt luminal entry of eosinophils. In conclusion, the present study demonstrates that acute allergic reactions initiate a prompt transepithelial migration of resident eosinophils. Our data further suggest that this response in part is initiated by the plasma exudation response, which may alter the transepithelial gradient of eosinophil chemoattractants including eotaxin. We propose that prompt eosinophil response is a significant component of the acute phase of allergic reactions when occurring in airways where these cells are already present in the mucosa.
authors.affiliation: Assoc. Prof. Department of Physiological Sciences, BMC F10, Lund University Hospital, 221 84, Lund, Sweden. jonas.erjefalt@mphy.lu.se
authors.forename: Jonas S
authors.initials: JS
authors.lastname: Erjefalt
authors.forename: Magnus
authors.initials: M
authors.lastname: Korsgren
authors.forename: Monika
authors.initials: M
authors.lastname: Malm-Erjefalt
authors.forename: Dolores M
authors.initials: DM
authors.lastname: Conroy
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Williams
authors.forename: Carl G A
authors.initials: CG
authors.lastname: Persson
mesh_terms: D000208:Acute Disease; D000707:Anaphylaxis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D001920:Bradykinin / Q000494:pharmacology; D001980:Bronchi / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D001993:Bronchodilator Agents / Q000494:pharmacology; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000235:genetics / Q000378:metabolism; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000276:immunology*; D004195:Disease Models, Animal; D004804:Eosinophils / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D004983:Ethanolamines / Q000494:pharmacology; D000068759:Formoterol Fumarate; D006168:Guinea Pigs; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D020545:Respiratory Mucosa / Q000276:immunology / Q000473:pathology / Q000503:physiopathology
chemical_list: D001993:Bronchodilator Agents; D054413:Chemokine CCL11; D019742:Chemokines, CC; D004983:Ethanolamines; D012333:RNA, Messenger; D001920:Bradykinin; D000068759:Formoterol Fumarate