| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Cell and Molecular Biology and
Department of Medicine, John A. Burns School of Medicine; and
Pacific Biosciences Research Center, University of Hawai’i, Honolulu HI 96813
Asthma is driven by allergic airway inflammation and involves increased levels of oxidative stress. This has led to speculation that antioxidants like selenium (Se) may play important roles in preventing or treating asthma. We fed diets containing low (0.08 parts per million), medium (0.25 parts per million), or high (2.7 parts per million) Se to female C57BL/6 mice and used an established OVA challenge protocol to determine the relationship between Se intake and the development of allergic airway inflammation. Results demonstrated that mice fed medium levels of Se had robust responses to OVA challenge in the lung as measured by lung cytokine levels, airway cellular infiltrate, eosinophilia, serum anti-OVA IgE, airway hyperreactivity, goblet cell hyperplasia, and phosphorylated STAT-6 levels in the lung. In contrast, responses to OVA challenge were less robust in mice fed low or high levels of Se. In particular, mice fed low Se chow showed significantly lower responses compared with mice fed medium Se chow for nearly all readouts. We also found that within the medium Se group the expression of lung glutathione peroxidase-1 and liver selenoprotein P were increased in OVA-challenged mice compared with PBS controls. These data suggest that Se intake and allergic airway inflammation are not related in a simple dose-response manner, which may explain the inconsistent results obtained from previous descriptive studies in humans. Also, our results suggest that certain selenoproteins may be induced in response to Ag challenges within the lung.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This publication was made possible by Grant 2 G12 RR003061-21 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. This work was also supported by NIH Grant R01 DK52963 and a Hawai’i Community Foundation Grant.
2 Address correspondence and reprint requests to Dr. Peter R. Hoffmann, Cell and Molecular Biology Department, University of Hawai’i, 651 Ilalo Street, Honolulu, HI 96813. E-mail address: peterh{at}pbrc.hawaii.edu
3 Abbreviations used in this paper: AHR, airway hyperactivity; BAL, bronchoalveolar lavage; GPX, glutathione peroxidase; log PC200, logarithm of the dose of acetylcholine required for a 200% increase in pulmonary resistance above baseline; pSTAT-6, phosphorylated STAT-6; ROS, reactive oxygen species; ppm, parts per million; SelP, selenoprotein P.
This article has been cited by other articles:
|
|
 |
|
  R. K. Shrimali, R. D. Irons, B. A. Carlson, Y. Sano, V. N. Gladyshev, J. M. Park, and D. L. Hatfield Selenoproteins Mediate T Cell Immunity through an Antioxidant Mechanism J. Biol. Chem., July 18, 2008; 283(29): 20181 - 20185. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
