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Ambroxol suppresses influenza-virus proliferation in the mouse airway by increasing antiviral factor levels

¹ Division of Enzyme Chemistry, Institute for Enzyme Research, The University of Tokushima, Tokushima and ² Dept of Microbiology, Kawasaki Medical School, Kurashiki, Japan

CORRESPONDENCE: H. Kido, Division of Enzyme Chemistry, Institute for Enzyme Research, The University of Tokushima, Kuramoto-cho 3-18-15, Tokushima, 770-8503, Japan. Fax: 81 886337425. E-mail: kido@ier.tokushima-u.ac.jp

Keywords: ambroxol, cytokine, immunoglobulin-A, influenza-A virus, mucus protease inhibitor, pulmonary surfactant protein A

Received: June 15, 2001
Accepted November 13, 2001

This study was supported by a grant-in-aid from the Ministry of Education, Science and Culture of Japan (No. 10557033).

The protective effect of ambroxol, a mucolytic agent which has antioxidant properties and stimulates the release of pulmonary surfactant, against influenza-virus proliferation in the airway was investigated in mice.

Ambroxol or the vehicle was administered intraperitoneally twice a day for 5–7 days to mice shortly after intranasal infection with a lethal dose of influenza A/Aichi/68 (H3N2) virus, and the survival rate, virus titre and levels of factors regulating virus proliferation in the airway fluid were analysed.

Ambroxol significantly suppressed virus multiplication and improved the survival rate of mice. The effect of ambroxol reached a peak at 10 mg·kg^–1·day^–1, higher doses being less effective. Ambroxol stimulated the release of suppressors of influenza-virus multiplication, such as pulmonary surfactant, mucus protease inhibitor, immunoglobulin (Ig)-A and IgG, although it stimulated the release of a trypsin-type protease that potentiates virus proliferation. In addition, ambroxol transiently suppressed release of the cytokines, tumour necrosis factor-, interferon- and interleukin-12, into airway fluid.

Although ambroxol had several negative effects on the host defence system, overall it strikingly increased the concentrations of suppressors of influenza-virus multiplication in the airway.

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