Jun N-terminal protein kinase enhances middle ear mucosal proliferation during bacterial otitis media
(2007) In Infection and Immunity 75(5). p.2562-2571- Abstract
- Mucosal hyperplasia is a characteristic component of otitis media. The present study investigated the participation of signaling via the Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase in middle ear mucosal hyperplasia in animal models of bacterial otitis media. Otitis media was induced by the inoculation of nontypeable Haemophilus influenzae into the middle ear cavity. Western blotting revealed that phosphorylation of JNK isoforms in the middle ear mucosa preceded but paralleled mucosal hyperplasia in this in vivo rat model. Nuclear JNK phosphorylation was observed in many cells of both the mucosal epithelium and stroma by immunohistochemistry. In an in vitro model of primary rat middle ear mucosal explants,... (More)
- Mucosal hyperplasia is a characteristic component of otitis media. The present study investigated the participation of signaling via the Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase in middle ear mucosal hyperplasia in animal models of bacterial otitis media. Otitis media was induced by the inoculation of nontypeable Haemophilus influenzae into the middle ear cavity. Western blotting revealed that phosphorylation of JNK isoforms in the middle ear mucosa preceded but paralleled mucosal hyperplasia in this in vivo rat model. Nuclear JNK phosphorylation was observed in many cells of both the mucosal epithelium and stroma by immunohistochemistry. In an in vitro model of primary rat middle ear mucosal explants, bacterially induced mucosal growth was blocked by the Rac/Cdc42 inhibitor Clostridium difficile toxin B, the mixed-lineage kinase inhibitor CEP11004, and the JNK inhibitor SP600125. Finally, the JNK inhibitor SP600125 significantly inhibited mucosal hyperplasia during in vivo bacterial otitis media in guinea pigs. Inhibition of JNK in vivo resulted in a diminished proliferative response, as shown by a local decrease in proliferating cell nuclear antigen protein expression by immunohistochemistry. We conclude that activation of JNK is a critical pathway for bacterially induced mucosal hyperplasia during otitis media, influencing tissue proliferation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/660484
- author
- Furukawa, Masayuki ; Ebmeyer, Joerg ; Pak, Kwang ; Austin, Darrell A. ; Melhus, Åsa LU ; Webster, Nicholas J. G. and Ryan, Allen F.
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Infection and Immunity
- volume
- 75
- issue
- 5
- pages
- 2562 - 2571
- publisher
- American Society for Microbiology
- external identifiers
-
- wos:000246345000055
- scopus:34248370548
- ISSN
- 1098-5522
- DOI
- 10.1128/IAI.01656-06
- language
- English
- LU publication?
- yes
- id
- a00dabe6-cdbe-4e7d-99a7-7122e684106a (old id 660484)
- date added to LUP
- 2016-04-01 12:28:16
- date last changed
- 2022-03-21 04:49:24
@article{a00dabe6-cdbe-4e7d-99a7-7122e684106a,
abstract = {{Mucosal hyperplasia is a characteristic component of otitis media. The present study investigated the participation of signaling via the Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase in middle ear mucosal hyperplasia in animal models of bacterial otitis media. Otitis media was induced by the inoculation of nontypeable Haemophilus influenzae into the middle ear cavity. Western blotting revealed that phosphorylation of JNK isoforms in the middle ear mucosa preceded but paralleled mucosal hyperplasia in this in vivo rat model. Nuclear JNK phosphorylation was observed in many cells of both the mucosal epithelium and stroma by immunohistochemistry. In an in vitro model of primary rat middle ear mucosal explants, bacterially induced mucosal growth was blocked by the Rac/Cdc42 inhibitor Clostridium difficile toxin B, the mixed-lineage kinase inhibitor CEP11004, and the JNK inhibitor SP600125. Finally, the JNK inhibitor SP600125 significantly inhibited mucosal hyperplasia during in vivo bacterial otitis media in guinea pigs. Inhibition of JNK in vivo resulted in a diminished proliferative response, as shown by a local decrease in proliferating cell nuclear antigen protein expression by immunohistochemistry. We conclude that activation of JNK is a critical pathway for bacterially induced mucosal hyperplasia during otitis media, influencing tissue proliferation.}},
author = {{Furukawa, Masayuki and Ebmeyer, Joerg and Pak, Kwang and Austin, Darrell A. and Melhus, Åsa and Webster, Nicholas J. G. and Ryan, Allen F.}},
issn = {{1098-5522}},
language = {{eng}},
number = {{5}},
pages = {{2562--2571}},
publisher = {{American Society for Microbiology}},
series = {{Infection and Immunity}},
title = {{Jun N-terminal protein kinase enhances middle ear mucosal proliferation during bacterial otitis media}},
url = {{http://dx.doi.org/10.1128/IAI.01656-06}},
doi = {{10.1128/IAI.01656-06}},
volume = {{75}},
year = {{2007}},
}