A role for dietary selenium and selenoproteins in allergic airway inflammation.
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.
Hoffmann
Peter R
PR
Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i, 651 Halo Street, Honolulu, HI 96813, USA. peterh@pbrc.hawaii.edu
Jourdan-Le Saux
Claude
C
Hoffmann
Fukun W
FW
Chang
Peter S
PS
Bollt
Oana
O
He
Qingping
Q
Tam
Elizabeth K
EK
Berry
Marla J
MJ
D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D004032:Diet; D005260:Female; D005979:Glutathione Peroxidase / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000276:immunology; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis; D008168:Lung / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D010766:Phosphorylation; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D050800:STAT6 Transcription Factor / Q000378:metabolism; D012643:Selenium / Q000008:administration & dosage*; D051149:Selenoprotein P / Q000235:genetics / Q000378:metabolism*; D018418:Th2 Cells / Q000276:immunology; D000094765:Glutathione Peroxidase GPX1
D016207:Cytokines; D053645:Interleukin-2 Receptor alpha Subunit; D012333:RNA, Messenger; D050800:STAT6 Transcription Factor; D051149:Selenoprotein P; D007073:Immunoglobulin E; D010047:Ovalbumin; D005979:Glutathione Peroxidase; D012643:Selenium; D000094765:Glutathione Peroxidase GPX1; C000722068:Gpx1 protein, mouse