title: Upregulated response to chemokines in oxidative metabolism of eosinophils in asthma and allergic rhinitis.
abstract: Reactive oxygen species (ROS) from eosinophils are known to cause tissue damage in allergic inflammation. CC chemokines, especially eotaxin and regulated on activation, normal T-cell expressed and secreted (RANTES), are involved not only in chemotaxis but also in eosinophil activation, such as ROS production. It has been shown that eosinophils from allergic patients are not functionally equivalent to those from normal subjects. In the present study, the characteristics of chemokine-primed ROS production in eosinophils from allergic patients and normal controls were compared. After pretreatment with chemokines, eosinophils were stimulated with calcium ionophore A23187. ROS production by eosinophils was measured using luminol-dependent chemiluminescence. Both RANTES and eotaxin exhibited a priming effect on calcium ionophore-induced ROS production from eosinophils. Despite there being no difference in expression of CC chemokine receptor 3, the priming effect of RANTES and eotaxin was significantly enhanced in eosinophils from the patients. Interleukin-5 further enhanced the priming effect of chemokines in eosinophils from normal subjects, but not those from allergic subjects. The present results suggest an upregulated response to chemokines in eosinophils from allergic patients, and that interleukin-5 can induce a similar phenotype to that found in vivo in allergic patients.
authors.affiliation: Dept of Clinical and Laboratory Medicine, Akita University School of Medicine, Hondo, Akita, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Sannohe
authors.forename: T
authors.initials: T
authors.lastname: Adachi
authors.forename: K
authors.initials: K
authors.lastname: Hamada
authors.forename: K
authors.initials: K
authors.lastname: Honda
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: N
authors.initials: N
authors.lastname: Saito
authors.forename: C H
authors.initials: CH
authors.lastname: Cui
authors.forename: H
authors.initials: H
authors.lastname: Kayaba
authors.forename: K
authors.initials: K
authors.lastname: Ishikawa
authors.forename: J
authors.initials: J
authors.lastname: Chihara
mesh_terms: D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000378:metabolism*; D054413:Chemokine CCL11; D018946:Chemokine CCL5 / Q000494:pharmacology*; D019742:Chemokines, CC / Q000494:pharmacology*; D004804:Eosinophils / Q000187:drug effects* / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D066298:In Vitro Techniques; D015848:Interleukin-5 / Q000494:pharmacology; D008163:Luminescent Measurements; D008297:Male; D010084:Oxidation-Reduction / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000032:analysis; D012016:Reference Values; D012221:Rhinitis, Allergic, Perennial / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects* / Q000502:physiology*
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D019742:Chemokines, CC; D015848:Interleukin-5; D017382:Reactive Oxygen Species