ToxSci Advance Access originally published online on September 1, 2005
Toxicological Sciences 2005 88(2):420-433; doi:10.1093/toxsci/kfi311
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Arginase Activity Differs with Allergen in the Effector Phase of Ovalbumin- versus Trimellitic Anhydride-Induced Asthma
* Department of Biochemistry and Molecular Biology, Medical School Duluth, University of Minnesota, Duluth, Minnesota 55812; Department of Veterinary and Biomedical Science, College of Veterinary Medicine, University of Minnesota, St. Paul, Minnesota 55108; Department of Mathematics and Statistics, College of Science and Engineering, University of Minnesota, Duluth, Minnesota 55812; and Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California 95616
Received June 28, 2005; accepted August 30, 2005
Both trimellitic anhydride (TMA), a small molecular weight chemical, and ovalbumin (OVA), a reference protein allergen, cause asthma with eosinophilia. To test the hypothesis that different allergens elicit symptoms of asthma via different effector pathways, gene expression was compared in lungs of Balb/c mice sensitized with either TMA or OVA, followed by intratracheal challenge with TMA conjugated to mouse serum albumin (TMA-MSA) or OVA, respectively. Sensitized animals challenged with mouse serum albumin (MSA) alone were controls. Seventy-two hours after challenge, lung eosinophil peroxidase indicated that both allergens caused the same significant change in eosinophilia. Total RNA was isolated from lung lobes of 6–8 animals in each of four treatment groups and hybridized to Affymetrix U74Av2 GeneChips. False discovery rates (q-values) were calculated from an overall F test to identify candidate genes with differences in expression for the four groups. Using a q-value cutoff of 0.1, 853 probe sets had significantly different expression across the four treatment groups. Of these 853 probe sets, 376 genes had an Experimental/Control ratio of greater than 1.2 or less than 1/1.2 for either OVA- or TMA-treated animals, and 249 of the 376 genes were uniquely up- or down-regulated for OVA or TMA (i.e., differentially expressed with the allergen). qRT-PCR analysis of selected transcripts confirmed the gene expression analysis. Increases in both arginase transcript and enzyme activity were significantly greater in OVA-induced asthma compared to TMA-induced asthma. These data suggest that pathways of arginine metabolism and the importance of nitric oxide may differ in OVA- and TMA-induced asthma.
Key Words: rodent; eosinophils; allergy; lung; nitric oxide.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  H. Maarsingh, A. B. Zuidhof, I. S. T. Bos, M. van Duin, J.-L. Boucher, J. Zaagsma, and H. Meurs Arginase Inhibition Protects against Allergen-induced Airway Obstruction, Hyperresponsiveness, and Inflammation Am. J. Respir. Crit. Care Med., September 15, 2008; 178(6): 565 - 573. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Meurs, R. Gosens, and J. Zaagsma Airway hyperresponsiveness in asthma: lessons from in vitro model systems and animal models Eur. Respir. J., August 1, 2008; 32(2): 487 - 502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Takemoto, K. Ogino, M. Shibamori, T. Gondo, Y. Hitomi, T. Takigawa, D.-H. Wang, J. Takaki, H. Ichimura, Y. Fujikura, et al. Transiently, paralleled upregulation of arginase and nitric oxide synthase and the effect of both enzymes on the pathology of asthma Am J Physiol Lung Cell Mol Physiol, December 1, 2007; 293(6): L1419 - L1426. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Kouznetsova, C. E. Chwieralski, R. Balder, M. Hinz, A. Braun, N. Krug, and W. Hoffmann Induced Trefoil Factor Family 1 Expression by Trans-Differentiating Clara Cells in a Murine Asthma Model Am. J. Respir. Cell Mol. Biol., March 1, 2007; 36(3): 286 - 295. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. W. Luebke, M. P. Holsapple, G. S. Ladics, M. I. Luster, M. Selgrade, R. J. Smialowicz, M. R. Woolhiser, and D. R. Germolec Immunotoxicogenomics: The Potential of Genomics Technology in the Immunotoxicity Risk Assessment Process Toxicol. Sci., November 1, 2006; 94(1): 22 - 27. [Abstract] [Full Text] [PDF]
|
|