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Featured in Newsweek
"The Path of a Pandemic" http://www.newsweek.com/id/195692
Swine Influenza Virus: Zoonotic Potential and Vaccination Strategies for the Control of Avian and Swine Influenzas
Eileen Thacker and Bruce Janke
Last year researchers from Iowa State University in Ames warned that pigs located in industrial-scale farms were being subjected to influenza infections from farm poultry, wild birds and their human handlers. Writing in The Journal of Infectious Diseases, Eileen Thacker and Bruce Janke said, "As a result of the constantly changing genetic makeup of individual influenza viruses in pigs, the U.S. swine industry is continually scrambling to respond to the influenza viruses circulating within individual production systems."

15 April 2007

Volume 195, Number 8
The Journal of Infectious Diseases 2007;195:1189–1193
0022-1899/2007/19508-0017$15.00
DOI: 10.1086/512859
BRIEF REPORT

MyD88‐Dependent Immune Response Contributes to Hearing Loss in Experimental Pneumococcal Meningitis

Matthias Klein,1

Caroline Schmidt,1

Stefan Kastenbauer,1

Robert Paul,1

Carsten J. Kirschning,2

Hermann Wagner,2

Bernadette Popp,1

Hans‐Walter Pfister,1 and

Uwe Koedel1

1Department of Neurology, Klinikum Großhadern, Ludwig Maximilian University, and 2Institute of Medical Microbiology, Immunology, and Hygiene, Technical University, Munich, Germany

Hearing loss is one of the most common sequelae in survivors of pneumococcal meningitis, affecting up to 26% of them. Here, we established the first mouse model of meningitis‐associated hearing loss and investigated the role played by the Toll‐like receptor–associated adapter molecule MyD88. C57BL/6 mice were infected intracisternally by Streptococcus pneumoniae. By use of audiometry and histological analysis, cochleae were assessed in uninfected control mice during the acute stage and after recovery. MyD88‐deficient mice were analyzed 24 h after infection. Wild‐type mice lost hearing capacity to a significant degree, which was accompanied by a granulocytic cochlear inflammation. After recovery, hearing loss was still evident, and spiral ganglion neuronal loss, hair cell damage, and fibrocytic occlusion of the cochlea were observed. In contrast, mice lacking MyD88 developed significantly less hearing loss and had diminished cochlear inflammation. Our results strongly suggest a proinflammatory role for MyD88 in the initiation of the inflammatory response during pneumococcal meningitis–associated labyrinthitis.

Received 2 August 2006; accepted 24 October 2006; electronically published 5 March 2007.

Reprints or correspondence: Dr. Hans‐Walter Pfister, Dept. of Neurology, Ludwig Maximilian University, Marchioninistr. 15, 81377 Munich, Germany ().

Cited by

Matthias Klein, Bianca Obermaier, Barbara Angele, Hans-Walter Pfister, Hermann Wagner, Uwe Koedel, and Carsten J. Kirschning. (2008) Innate Immunity to Pneumococcal Infection of the Central Nervous System Depends on Toll-Like Receptor (TLR) 2 and TLR4. The Journal of Infectious Diseases 198:7, 1028-1036
Online publication date: 1-Oct-2008.
  • Potential conflicts of interest: none reported.

    Financial support: Friedrich‐Baur Stiftung (support to M.K.); Deutsche Forschungs‐Gemeinschaft (grant PF246/6‐2 to H.‐W.P. and SFB576/A5 to U.K.); Else Kroener‐Fresenius‐Foundation (support to U.K. and M.K.); Meningitis Research Foundation (grant 0611.0 to M.K.).

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