Heme Oxygenase (HO)-1 Is Upregulated in the Nasal Mucosa With Allergic Rhinitis

Authors

  • Ahmed Elhini MD,

    Corresponding author
    1. Department of Otorhinolaryngology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan
    • Dr. Ahmed Elhini, Department of Otorhinolaryngology, Juntendo University School of Medicine, 2-1-3 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
    Search for more papers by this author
  • Soha Abdelwahab MD, PhD,

    1. Division of Histology, Department of Cell Biology, Graduate School of Medical Science, Tohoku University, Sendai, Japan
    Search for more papers by this author
  • Katsuhisa Ikeda MD, PhD

    1. Department of Otorhinolaryngology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan
    Search for more papers by this author

  • This work was orally presented at the 6th International Academic Conference on Immuno- & Molecular Biology in Otorhinolaryngology, Jeju, South Korea, October 17–21, 2002.

Abstract

Background: Heme oxygenase (HO) is considered to be an antioxidant enzyme that catabolizes heme to produce carbon monoxide (CO) and biliverdin. Three isoforms of HO have been discovered. Recently, HO-1 has been found to be upregulated after allergic inflammations of the lower airway.

Objective: The objective of this study was to address the expression of HO isoenzymes 1 and 2 in the nasal mucosa of patients with allergic rhinitis as well as normal control subjects.

Methods: Nasal mucosa from 30 patients with persistent allergic rhinitis as well as from 10 normal volunteers was used in this study. We used immunofluorescent technique, Western blotting, and real-time quantitative polymerase chain reaction to localize and quantify the expression of these isoenzymes in normal and allergic human nasal tissues.

Results: We found that HO-1 is expressed in the epithelial cells of seromucinous glands and macrophages with significant upregulation of its glandular expression in allergic rhinitis but with no difference in its macrophage expression between the study groups in contrast to HO-2 that is expressed in the vascular endothelial lining cells as well as macrophages with no marked difference between the study groups.

Conclusion: We demonstrated that expression of HO-1, but not HO-2, was upregulated within the nasal tissues in allergic rhinitis inflammation, and understanding the induction of HO-1 expression may provide for better management of allergic rhinitis that involves oxidative stress.

Ancillary