Published ahead of print on June 16, 2005, doi:10.1165/rcmb.2005-0003OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 3, September 2005, 290-296 A more recent version of this article appeared on September 1, 2005
Submitted on January 4, 2005 IL-25 and IL-13 Production by Alveolar Macrophages in Response to ParticlesChun-Mi Kang1,1 Genome Research Center for Allergy and Respiratory Diseases, Soonchuhyang University Hospital, Bucheon, Gyeonggi Do, Korea, Republic of, 2 Division of Allergy and Respiratory Diseases, Soonchuhyang University Hospital, Bucheon, Gyeonggi Do, Korea, Republic of, 3 Genome Research Center for Allergy and Respiratory Diseases, Soonchuhyang University Hospital, Bucheon, Gyeonggi Do, Korea, Republic of; Division of Allergy and Respiratory Diseases, Soonchuhyang University Hospital, Bucheon, Gyeonggi Do, Korea, Republic of * To whom correspondence should be addressed. E-mail: mdcspark{at}unitel.co.kr.
Particle inhalation-induced lung inflammation acts as an adjuvant to allergens or respiratory viral infection in a process that is mediated by macrophages and epitheliums. The production of IL-4 and IL-13 by activated T cells is involved in the augmentation of Th2-type immune responses to particles, and IL-25 induces the synthesis of IL-4 and IL-13. However, whether IL-13 and IL-25 are directly regulated by particle instillation in the lung has not been studied. The aim of this study was to reveal particle induction of IL-13 and IL-25 in the lung. TiO2 instillation potently induced the mRNA expression for IL-25 and IL-13 in lung tissue extracts 24 hours after treatment, as compared to the sham group. Immunostaining for IL-25 and IL-13 showed strong positivity for macrophages in the inflammatory lung lesions of TiO2-treated rats. The alveolar macrophages expressed IL-25 and IL-13 24 hours after in vitro stimulation with TiO2 particles in dose- and time-dependent manners, with maximal induction at 24 and 48 hours post-stimulation, respectively. The sequence of the rat IL-25 gene is 95% homologous with the mouse IL-25 gene. These findings indicate that alveolar macrophages play an important role in particle-induced lung inflammation via direct induction of IL-13 and IL-25 production.
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