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Published ahead of print on June 9, 2005, doi:10.1165/rcmb.2004-0372OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 33, pp. 303-314, 2005
© 2005 American Thoracic Society
DOI: 10.1165/rcmb.2004-0372OC

Gob-5 Is Not Essential for Mucus Overproduction in Preclinical Murine Models of Allergic Asthma

Annette Robichaud*, Stephanie A. Tuck*, Stacia Kargman, John Tam, Elizabeth Wong, Mark Abramovitz, James Mortimer, Helen E. Burston, Paul Masson, Jeremy Hirota, Deborah Slipetz, Brian Kennedy, Gary O'Neill and Steven Xanthoudakis

Department of Biochemistry & Molecular Biology, and Pharmacology, Merck Frosst Centre for Therapeutic Research, Kirkland, Quebec, Canada

Correspondence and requests for reprints should be addressed to Steven Xanthoudakis, Ph.D., Department of Biochemistry and Molecular Biology, Merck Centre for Therapeutic Research, P.O. Box 1005, Pointe-Claire-Dorval, PQ, H9R 4P8 Canada. E-mail: steven_xanthoudakis{at}merck.com

Overexpression of Gob-5 has previously been linked to goblet cell metaplasia and mucin overproduction in both in vitro and in vivo model systems. In this study, Gob-5 knockout mice were generated and their phenotype was evaluated in two established preclinical models of allergic asthma. We sought to determine whether the Gob-5–null animals could produce less mucus in response to allergic challenge, and whether this would have any impact on reducing goblet cell metaplasia and airway inflammation. We found that in the absence of a proinflammatory stimulus we could not detect an overt phenotypic difference between age and sex-matched knockout and wild-type animals. Allergic challenge with ovalbumin or intranasal administration of interleukin-13 produced a robust allergic response that was similar regardless of genotype. In addition, siRNA-mediated knockdown of CLCA-1 in cultured lung epithelial cells failed to reduce mucin expression in vitro. Thus, in contrast to previously published reports, our findings show that Gob-5 expression is not essential for mucin overproduction in vitro or in murine models of allergic asthma. Furthermore, we have also exploited the use of gene expression array analysis to investigate the possibility that a compensatory mechanism, involving other genes, may act to override the requirement for Gob-5–mediated mucus overproduction.




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