Aquaporin-3 potentiates allergic airway inflammation in ovalbumin-induced murine asthma

Kohei Ikezoe, Toru Oga, Tetsuya Honda, Mariko Hara-Chikuma, Xiaojun Ma, Tatsuaki Tsuruyama, Kazuko Uno, Jun Ichi Fuchikami, Kiminobu Tanizawa, Tomohiro Handa, Yoshio Taguchi, Alan S. Verkman, Shuh Narumiya, Michiaki Mishima, Kazuo Chin

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


Oxidative stress plays a pivotal role in the pathogenesis of asthma. Aquaporin-3 (AQP3) is a small transmembrane water/glycerol channel that may facilitate the membrane uptake of hydrogen peroxide (H2O2). Here we report that AQP3 potentiates ovalbumin (OVA)-induced murine asthma by mediating both chemokine production from alveolar macrophages and T cell trafficking. AQP3 deficient (AQP3 -/-) mice exhibited significantly reduced airway inflammation compared to wild-type mice. Adoptive transfer experiments showed reduced airway eosinophilic inflammation in mice receiving OVA-sensitized splenocytes from AQP3 -/- mice compared with wild-type mice after OVA challenge, consistently with fewer CD4 + T cells from AQP3 -/- mice migrating to the lung than from wild-type mice. Additionally, in vivo and vitro experiments indicated that AQP3 induced the production of some chemokines such as CCL24 and CCL22 through regulating the amount of cellular H2O2 in M2 polarized alveolar macrophages. These results imply a critical role of AQP3 in asthma, and AQP3 may be a novel therapeutic target.

Original languageEnglish
Article number25781
JournalScientific reports
Publication statusPublished - 2016 May 11
Externally publishedYes

ASJC Scopus subject areas

  • General


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