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

Palacios, Sean D.; Pak, Kwang; Rivkin, Alexander Z; Kayali, Ayse G; Austen, Darrell; Aletsee, Christoph; Melhus, Åsa LU ; Webster, Nicholas J G and Ryan, Allen F. (2004) In Infection and Immunity 72(8). p.4662-4667
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Infection and Immunity
volume
72
issue
8
pages
4662 - 4667
publisher
American Society for Microbiology
external identifiers
  • wos:000222932600041
  • pmid:15271927
  • scopus:3342965776
ISSN
1098-5522
DOI
10.1128/IAI.72.8.4662-4667.2004
language
English
LU publication?
yes
id
c85763f7-7aff-4db5-8b14-8c3e50eee373 (old id 141844)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15271927&query_hl=57
date added to LUP
2007-07-26 14:19:54
date last changed
2017-12-10 03:41:28
@article{c85763f7-7aff-4db5-8b14-8c3e50eee373,
  abstract     = {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.},
  author       = {Palacios, Sean D. and Pak, Kwang and Rivkin, Alexander Z and Kayali, Ayse G and Austen, Darrell and Aletsee, Christoph and Melhus, Åsa and Webster, Nicholas J G and Ryan, Allen F.},
  issn         = {1098-5522},
  language     = {eng},
  number       = {8},
  pages        = {4662--4667},
  publisher    = {American Society for Microbiology},
  series       = {Infection and Immunity},
  title        = {Role of p38 Mitogen-Activated Protein Kinase in Middle Ear Mucosa Hyperplasia during Bacterial Otitis Media},
  url          = {http://dx.doi.org/10.1128/IAI.72.8.4662-4667.2004},
  volume       = {72},
  year         = {2004},
}