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Upregulated response to chemokines in oxidative metabolism of eosinophils in asthma and allergic rhinitis

Depts of ¹ Clinical and Laboratory Medicine and ² Oto-Rhino-Laryngology, Akita University School of Medicine, Akita, Japan

CORRESPONDENCE: J. Chihara, Dept of Clinical and Laboratory Medicine, Akita University School of Medicine, Hondo, Akita 010-8543, Japan. Fax: 81 188362624. E-mail: chihara@hos.akita-u.ac.jp

Keywords: CC chemokine receptor 3, eosinophils, eotaxin, interleukin-5, reactive oxygen species, regulated on activation, normal T-cell expressed and secreted

Received: April 4, 2002
Accepted January 14, 2003

This study was supported by grants-in-aid for Scientific Research from the Ministry of Education and Science, and the Ministry of Health and Welfare (both Tokyo, Japan).

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.

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