TNFA deletion alters apoptosis as well as caspase 3 and 4 expression during otitis media

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  • Ebmeyer, Joerg
    • Other Affiliation: Department of Otorhinolaryngology, Head and Neck Surgery Klinikum Bielefeld (Academic Teaching Hospital University of Münster), Bielefeld, Germany
  • Leichtle, Anke
    • Other Affiliation: Department of Surgery, Division of Otolaryngology, University of California, San Diego School of Medicine and Department of Veterans Affairs Medical Center, La Jolla, California, USA
  • Hernandez, Michelle
    • Other Affiliation: Department of Medicine, Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, California, USA
  • Ebmeyer, Umay
    • Other Affiliation: Department of Obstetrics and Gynecology Städtische Klinikum Bielefeld (Academic Teaching Hospital University of Münster), Bielefeld, Germany
  • Husseman, Jacob
    • Other Affiliation: Department of Surgery, Division of Otolaryngology, University of California, San Diego School of Medicine and Department of Veterans Affairs Medical Center, La Jolla, California, USA
  • Pak, Kwang
    • Other Affiliation: Department of Surgery, Division of Otolaryngology, University of California, San Diego School of Medicine and Department of Veterans Affairs Medical Center, La Jolla, California, USA
  • Sudhoff, Holger
    • Other Affiliation: Department of Otorhinolaryngology, Head and Neck Surgery Klinikum Bielefeld (Academic Teaching Hospital University of Münster), Bielefeld, Germany
  • Broide, David
    • Other Affiliation: Department of Medicine, Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, California, USA
  • Wasserman, Stephen I
    • Other Affiliation: Department of Medicine, Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, California, USA
  • Ryan, Allen F
    • Other Affiliation: Department of Surgery, Division of Otolaryngology, University of California, San Diego School of Medicine and Department of Veterans Affairs Medical Center, La Jolla, California, USA
Abstract
  • Abstract Background Tumor necrosis factor (TNFA) is the canonical member of the TNF superfamily, which plays a major role in both inflammation and apoptosis. To evaluate the role of TNFs in otitis media (OM), the most common disease of childhood, we evaluated middle ear (ME) expression of genes encoding the TNF and TNF receptor superfamilies during bacterial OM in the mouse, characterized OM in TNFA-deficient mice, and assessed apoptosis during OM in normal versus TNF-deficient MEs. Results TNFs and TNF receptors were broadly regulated during OM, with TNFA showing the highest level of up-regulation. TNF deficient mice exhibited mucosal hyperplasia even in the absence of infection and exuberant growth of the mucosa during OM, including the formation of mucosal polyps. Mucosal recovery during OM was also delayed, in parallel with a delay in mucosal apoptosis and reduced caspase gene expression. Conclusions The TNF and TNF receptor superfamilies mediate both inflammation and apoptosis during OM. TNF appears to be critical for the maintenance of mucosal architecture in both the normal and infected ME, since excessive accumulation of mucosal tissue is seen in TNFA-/- MEs both before and after bacterial inoculation of the ME. TNFA is also required for appropriate regulation of caspase genes.
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  • Article
Rights statement
  • In Copyright
Rights holder
  • Joerg Ebmeyer et al.; licensee BioMed Central Ltd.
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Journal title
  • BMC Immunology
Journal volume
  • 12
Journal issue
  • 1
Page start
  • 12
Language
  • English
Is the article or chapter peer-reviewed?
  • Yes
ISSN
  • 1471-2172
Bibliographic citation
  • BMC Immunology. 2011 Jan 26;12(1):12
Publisher
  • BioMed Central Ltd
Access right
  • Open Access
Date uploaded
  • August 23, 2012

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file details 1471-2172-12-12.pdf 2019-05-07 Public Download
file details Table S1. Fold expression data derived from gene arrays, for the TNF and TNFR family genes presented graphically in Figure 1, including variability (Range) and significance (P-value). 2019-05-07 Public Download
file details 1471-2172-12-12.xml 2019-05-07 Public Download