Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading

Shinsuke Nakazawa, Takatoshi Shimauchi, Atsuko Funakoshi, Masahiro Aoshima, Pawit Phadungsaksawasdi, Jun ichi Sakabe, Sanki Asakawa, Noriyasu Hirasawa, Taisuke Ito, Yoshiki Tokura

Research output: Contribution to journalArticlepeer-review

Abstract

Suprabasin (SBSN) is expressed not only in epidermis but also in epithelial cells of the upper digestive tract where metals such as nickel are absorbed. We have recently shown that SBSN level is decreased in the stratum corneum and serum of atopic dermatitis (AD) patients, especially in intrinsic AD, which is characterized by metal allergy. By using SBSN-null (Sbsn–/–) mice, this study was conducted to investigate the outcome of SBSN deficiency in relation to AD. Sbsn–/– mice exhibited skin barrier dysfunction on embryonic day 16.5, but after birth, their barrier function was not perturbed despite the presence of ultrastructural changes in stratum corneum and keratohyalin granules. Sbsn–/– mice showed a comparable ovalbumin-specific skin immune response to wild type (WT) mice and rather lower contact hypersensitivity (CHS) responses to haptens than did WT mice. The blood nickel level after oral feeding of nickel was significantly higher in Sbsn–/– mice than in WT mice, and CHS to nickel was elevated in Sbsn–/– mice under nickel-loading condition. Our study suggests that the completely SBSN deficient mice retain normal barrier function, but harbor abnormal upper digestive tract epithelium that promotes nickel absorption and high CHS to nickel, sharing the features of intrinsic AD.

Original languageEnglish
Article number14559
JournalScientific reports
Volume10
Issue number1
DOIs
Publication statusPublished - 2020 Dec 1

ASJC Scopus subject areas

  • General

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