Published ahead of print on March 9, 2006, doi:10.1165/rcmb.2005-0134OC Am. J. Respir. Cell Mol. Biol., Volume 35, Number 1, July 2006, 103-109 A more recent version of this article appeared on July 1, 2006
Submitted on April 11, 2005 Role of ECF-L on Airway Hyperresponsiveness in a Murine Model of Allergic AsthmaHiroki Iwashita1*,1 Pharmacology Research Laboratories III, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Tsukuba, Ibaraki, Japan, 2 Pharmacology Research Laboratories II, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Tsukuba, Ibaraki, Japan * To whom correspondence should be addressed. E-mail: Iwashita_Hiroki{at}takeda.co.jp.
Airway hyperresponsiveness (AHR) is an important feature of bronchial asthma. Although the incidence of AHR has both 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 (SSH) analysis revealed that 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 DIG-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 airway hyperresponsiveness and eosinophil infiltration. These results indicate that ECF-L may play a critical role in allergic inflammation and bronchial asthma.
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