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Published ahead of print on March 9, 2006, doi:10.1165/rcmb.2005-0134OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 35, pp. 103-109, 2006
© 2006 American Thoracic Society
DOI: 10.1165/rcmb.2005-0134OC

Role of Eosinophil Chemotactic Factor by T Lymphocytes on Airway Hyperresponsiveness in a Murine Model of Allergic Asthma

Hiroki Iwashita, Shigeru Morita, Yoji Sagiya and Atsushi Nakanishi

Pharmacology Research Laboratories II and III, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Ibaraki, Japan

Correspondence and requests for reprints should be addressed to Hiroki Iwashita, Pharmacology Research Laboratories III, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, 10 Wadai, Tsukuba, Ibaraki, 300-4293, Japan. E-mail: Iwashita_Hiroki{at}takeda.co.jp

Airway hyperresponsiveness (AHR) is an important feature of bronchial asthma. Although the incidence of AHR has genetic and environmental components, the mechanism of AHR in asthma remains unclear. The identification of genes that are preferentially expressed in a murine model of AHR could help elucidate the molecular mechanisms of this pulmonary pathology. Suppressive subtractive hybridization analysis revealed that eosinophil chemotactic factor by T lymphocytes (ECF-L), a mouse chitinase family protein, was selectively expressed in the lungs of mice with AHR. Induction of ECF-L expression was observed soon after allergen exposure but before the onset of airway inflammation. Cell-specific ECF-L expression was examined by in situ hybridization using digoxigenin-labeled antisense RNA probes and immunofluorescence staining. The assay revealed that the ECF-L–expressing cells in the lungs of the AHR-model mice are alveolar macrophages. Intratracheal administration of an adenoviral vector that expressed antisense ECF-L RNA (Ad-ECF-L-AS) suppressed AHR and eosinophil infiltration. These results indicate that ECF-L may play a critical role in allergic inflammation and bronchial asthma.

Key Words: eosinophil chemotactic factor by T lymphocytes (ECF-L) • airway hyperresponsiveness (AHR) • eosinophil infiltration




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