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Infection and Immunity, August 2004, p. 4662-4667, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4662-4667.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Role of p38 Mitogen-Activated Protein Kinase in Middle Ear Mucosa Hyperplasia during Bacterial Otitis Media

Sean D. Palacios,1,{dagger} Kwang Pak,1,2,{dagger} Alexander Z. Rivkin,1 Ayse G. Kayali,3 Darrell Austen,3 Christoph Aletsee,1,4 Åsa Melhus,1,5 Nicholas J. G. Webster,2,3 and Allen F. Ryan1,2*

Departments of Surgery/Otolaryngology,1 Medicine,3 University of California, San Diego, and VA Medical Center, La Jolla, California,2 Department of Otolaryngology, University of Wuerzburg, Wuerzburg, Germany,4 Department of Microbiology, University of Lund, Lund, Sweden5

Received 20 February 2004/ Returned for modification 30 March 2004/ Accepted 22 April 2004

Hyperplasia of the middle ear mucosa contributes to the sequelae of acute otitis media. Understanding the signal transduction pathways that mediate hyperplasia could lead to the development of new therapeutic interventions for this disease and its sequelae. Endotoxin derived from bacteria involved in middle ear infection can contribute to the hyperplastic response. The p38 mitogen-activated protein kinase (MAPK) is known to be activated by endotoxin as well as cytokines and other inflammatory mediators that have been documented in otitis media. We assessed the activation of p38 in the middle ear mucosa of an in vivo rat bacterial otitis media model. Strong activity of p38 was observed 1 to 6 h after bacterial inoculation. Activity continued at a lower level for at least 7 days. The effects of p38 activation were assessed using an in vitro model of rat middle ear mucosal hyperplasia in which mucosal growth is stimulated by nontypeable Haemophilus influenzae during acute otitis media. Hyperplastic mucosal explants treated with the p38{alpha} and p38ß inhibitor SB203580 demonstrated significant inhibition of otitis media-stimulated mucosal growth. The results of this study suggest that intracellular signaling via p38 MAPK influences the hyperplastic response of the middle ear mucosa during bacterial otitis media.

* Corresponding author. Mailing address: Department of Surgery/Otolaryngology, Univ. of California-San Diego School of Medicine, Fir Bldg., Rm. 106, 9500 Gilman Dr. #0666, La Jolla, CA 92037. Phone: (858) 534-4594. Fax: (858) 534-5319. E-mail: aryan{at}ucsd.edu.

Editor: D. L. Burns

{dagger} S.D.P. and K.P. contributed equally to the manuscript.

Infection and Immunity, August 2004, p. 4662-4667, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4662-4667.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Furukawa, M., Ebmeyer, J., Pak, K., Austin, D. A., Melhus, A., Webster, N. J. G., Ryan, A. F. (2007). Jun N-Terminal Protein Kinase Enhances Middle Ear Mucosal Proliferation during Bacterial Otitis Media. Infect. Immun. 75: 2562-2571 [Abstract] [Full Text]  


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