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Published ahead of print on July 25, 2003, doi:10.1164/rccm.200304-548OC

Am. J. Respir. Crit. Care Med., Volume 168, Number 7, October 2003, 783-789

A more recent version of this article appeared on October 1, 2003
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Submitted on April 21, 2003
Accepted on July 16, 2003

SP-D Regulates Airway Function and Allergic Inflammation Through Regulation of Macrophage Function

Katsuyuki Takeda, Nobuaki Miyahara, Yeong-Ho Rha, Christian Taube, Eun-Seok Yang, Anthony Joetham, Taku Kodama, Annette Balhorn, Azzeddine Dakhama, Catherine Duez, Amanda Evans, Dennis R Voelker, and Erwin W Gelfand*

* To whom correspondence should be addressed. E-mail: gelfande{at}njc.org.

The lung collectin, SP-D, is an important component of the innate immune response but is also thought to play a role in other regulatory aspects of immune and inflammatory responses within the lung. The role of SP-D in the development of allergen-induced airway inflammation and hyperresponsiveness (AHR) is not well-defined. SP-D levels progressively increased up to 48 hrs following allergen challenge of sensitized mice and then subsequently decreased. The levels of SP-D paralleled the development of airway eosinophilia and AHR. To determine if this association was functionally relevant, mice were administered rat SP-D (rSP-D) intratracheally. When given to sensitized mice prior to challenge, AHR and eosinophilia were reduced by rSP-D in a dose-dependent manner, but not by mutant rSP-D. rSP-D administration resulted in increased levels of IL-10, IL-12 and interferon-{gamma} (IFN-{gamma}) in BAL fluid and reduced goblet cell hyperplasia. Culture of alveolar macrophages together with SP-D and allergen resulted in increased production of IL-10, IL-12 and IFN-{gamma}. These results indicate that SP-D can (negatively) regulate the development of AHR and airway inflammation following airway challenge of sensitized mice, at least in part, by modulating the function of alveolar macrophages.
Key words: Surfactant protein D, airway hyperresponsiveness, eosinophils, macrophages




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