Abstract |
The effects of selective CC chemokine receptor (CCR)-3 antagonists on antigen-induced leukocyte accumulation in the lungs of mice adoptively transferred with in vitro-differentiated T(h)1 and T(h)2 were investigated. Inhalation of antigen by mice injected with T(h)1 and T(h)2 initiated the migration of T cells themselves into the lungs. Subsequently, neutrophils massively accumulated in T(h)1-transferred mice, whereas eosinophil infiltration was specifically induced by T(h)2. CCR3 antagonists, SB-297006 and/or SB-328437, suppressed antigen-induced accumulation of T(h)2 as well as eosinophils in the lungs, whereas they failed to affect T(h)1-mediated airway inflammation. Not only T(h)2 and eosinophil infiltration but also cellular mobilization in T(h)1-transferred mice was attenuated by an anti- CC chemokine ligand-11 antibody. CCR3 antagonists reduced chemokine production in the lungs of mice transferred with T(h)2 but not T(h)1, suggesting that down-regulation of chemokine synthesis is involved in the selective inhibition of T(h)2-mediated eosinophil infiltration by CCR3 antagonists.
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Authors | Akio Mori, Koji Ogawa, Koichiro Someya, Yuichi Kunori, Daisuke Nagakubo, Osamu Yoshie, Fujiko Kitamura, Takachika Hiroi, Osamu Kaminuma |
Journal | International immunology
(Int Immunol)
Vol. 19
Issue 8
Pg. 913-21
(Aug 2007)
ISSN: 0953-8178 [Print] England |
PMID | 17804691
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzamides
- Ccr3 protein, mouse
- Naphthalenes
- Receptors, CCR3
- SB 297006
- SB 328437
- Phenylalanine
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Topics |
- Animals
- Benzamides
(pharmacology)
- Bronchial Hyperreactivity
(immunology)
- Chemotaxis, Leukocyte
(drug effects)
- Eosinophils
(immunology, metabolism)
- Inflammation
(immunology, metabolism)
- Lung
(drug effects, immunology)
- Mice
- Naphthalenes
(pharmacology)
- Neutrophils
(immunology, metabolism)
- Phenylalanine
(analogs & derivatives, pharmacology)
- Receptors, CCR3
(antagonists & inhibitors, immunology, metabolism)
- Th1 Cells
(immunology, metabolism)
- Th2 Cells
(immunology, metabolism)
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