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Pili play an important role in enhancing the bacterial clearance from the middle ear in a mouse model of acute otitis media with Moraxella catarrhalis.

Authors :
Toshiaki Kawano
Takashi Hirano
Satoru Kodama
Marcelo Takahiro Mitsui
Kamruddin Ahmed
Akira Nishizono
Masashi Suzuki
Source :
Pathogens & Disease. Mar2013, Vol. 67 Issue 2, p119-131. 13p. 1 Color Photograph, 4 Charts, 8 Graphs.
Publication Year :
2013

Abstract

Moraxella catarrhalis is a Gram-negative aerobic diplococcus that is currently the third most frequent cause of bacterial acute otitis media (AOM) in children. In this study, we developed an experimental murine AOM model by inoculating M. catarrhalis in the middle ear bulla and studied the local response to this inoculation, and modulation of its course by the pili of M. catarrhalis. The pili-positive and pili-negative M. catarrhalis showed differences in bacterial clearance and infiltration of inflammatory cells in the middle ear. Pili-negative M. catarrhalis induced a more delayed and prolonged immune response in the middle ear than that of pili-positive M. catarrhalis. TLR2, -4, -5 and -9 mRNA expression was upregulated in neutrophils that infiltrated the middle ear cavity during AOM caused by both pili-positive and pili-negative bacteria. TLR5 mRNA expression and TLR5 protein in the neutrophils were induced more robustly by pili-positive M. catarrhalis. This immune response is likely to be related to neutrophil function such as toll-like 5-dependent phagocytosis. Our results show that mice may provide a useful AOM model for studying the role of M. catarrhalis. Furthermore, we show that pili play an important role in enhancing M. catarrhalis clearance from the middle ear that is probably mediated through neutrophil-dependent TLR5 signaling. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
2049632X
Volume :
67
Issue :
2
Database :
Academic Search Index
Journal :
Pathogens & Disease
Publication Type :
Academic Journal
Accession number :
131850722
Full Text :
https://doi.org/10.1111/2049-632X.12025