Upregulation of interleukin-13 receptor chains in bronchial smooth muscle tissues of mouse experimental asthma
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Updated: Jun 14, 2026

A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
Published on: April 13, 2010
Yoshihiko Chiba1, Satoshi Onoda, Michiko Todoroki
1Department of Pharmacology, School of Pharmacy, Hoshi University, Tokyo, Japan. chiba@hoshi.ac.jp
Abstract:
Interleukin-13 (IL-13) is believed to be a central mediator of the induction of airway hyperresponsiveness (AHR), one of the characteristic features of allergic bronchial asthma. The IL-13-mediated events are mainly generated by its binding to functional IL-13 receptor, IL13Ralpha1 chain. In the present study, the changes in the levels of IL-13 receptors in bronchial smooth muscles were determined in mice with AHR induced by antigen inhalation. Mice were sensitized and repeatedly challenged with ovalbumin antigen. Total RNAs of the left main bronchi were extracted, and real-time RT-PCR analyses for IL13Ralpha1 and IL13Ralpha2 chains were conducted. As a result, both the receptor chains were significantly increased in the diseased bronchial smooth muscle. The time-course analyses revealed that the peaks of IL13Ralpha1 and IL13Ralpha2 upregulations were at 6 hour and 3-12 hour after the last antigen inhalation, respectively. It is thus possible that the IL-13-mediated signaling in bronchial smooth muscle is considerably augmented by the upregulations of IL-13 itself and its functional IL13Ralpha1 receptor in allergic asthmatics.
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