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Vinpocetine Inhibits Streptococcus pneumoniae–Induced Upregulation of Mucin MUC5AC Expression via Induction of MKP-1 Phosphatase in the Pathogenesis of Otitis Media

Ji-Yun Lee, Kensei Komatsu, Byung-Cheol Lee, Masanori Miyata, Ashley O’Neill Bohn, Haidong Xu, Chen Yan and Jian-Dong Li
J Immunol May 13, 2015, 1401489; DOI: https://doi.org/10.4049/jimmunol.1401489
Ji-Yun Lee
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Kensei Komatsu
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Byung-Cheol Lee
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Masanori Miyata
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Ashley O’Neill Bohn
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Haidong Xu
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Chen Yan
†Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642
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Jian-Dong Li
*Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; and
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Abstract

Mucin overproduction is a hallmark of otitis media (OM). Streptococcus pneumoniae is one of the most common bacterial pathogens causing OM. Mucin MUC5AC plays an important role in mucociliary clearance of bacterial pathogens. However, if uncontrolled, excessive mucus contributes significantly to conductive hearing loss. Currently, there is a lack of effective therapeutic agents that suppress mucus overproduction. In this study, we show that a currently existing antistroke drug, vinpocetine, a derivative of the alkaloid vincamine, inhibited S. pneumoniae–induced mucin MUC5AC upregulation in cultured middle ear epithelial cells and in the middle ear of mice. Moreover, vinpocetine inhibited MUC5AC upregulation by inhibiting the MAPK ERK pathway in an MKP-1–dependent manner. Importantly, ototopical administration of vinpocetine postinfection inhibited MUC5AC expression and middle ear inflammation induced by S. pneumoniae and reduced hearing loss and pneumococcal loads in a well-established mouse model of OM. Thus, these studies identified vinpocetine as a potential therapeutic agent for inhibiting mucus production in the pathogenesis of OM.

Footnotes

  • This work was supported by National Institutes of Health Grants DC005843, DC004562, and GM107529 (to J.-D.L.) and HL111291 and HL088400 (to C.Y.). J.-D.L. is a Georgia Research Alliance Eminent Scholar in Inflammation and Immunity.

  • The online version of this article contains supplemental material.

  • Received June 11, 2014.
  • Accepted April 19, 2015.
  • Copyright © 2015 by The American Association of Immunologists, Inc.

This article is distributed under The American Association of Immunologists, Inc., Reuse Terms and Conditions for Author Choice articles.

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The Journal of Immunology: 209 (1)
The Journal of Immunology
Vol. 209, Issue 1
1 Jul 2022
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Vinpocetine Inhibits Streptococcus pneumoniae–Induced Upregulation of Mucin MUC5AC Expression via Induction of MKP-1 Phosphatase in the Pathogenesis of Otitis Media
Ji-Yun Lee, Kensei Komatsu, Byung-Cheol Lee, Masanori Miyata, Ashley O’Neill Bohn, Haidong Xu, Chen Yan, Jian-Dong Li
The Journal of Immunology May 13, 2015, 1401489; DOI: 10.4049/jimmunol.1401489

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Vinpocetine Inhibits Streptococcus pneumoniae–Induced Upregulation of Mucin MUC5AC Expression via Induction of MKP-1 Phosphatase in the Pathogenesis of Otitis Media
Ji-Yun Lee, Kensei Komatsu, Byung-Cheol Lee, Masanori Miyata, Ashley O’Neill Bohn, Haidong Xu, Chen Yan, Jian-Dong Li
The Journal of Immunology May 13, 2015, 1401489; DOI: 10.4049/jimmunol.1401489
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