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

BMC Immunology

Research Article

David Broide¹  Michelle Hernandez¹  Stephen I Wasserman¹  Umay Ebmeyer²  Joerg Ebmeyer³  Holger Sudhoff³  Anke Leichtle⁴  Jacob Husseman⁴  Allen F Ryan⁴  Kwang Pak⁴ 

[1] Department of Medicine, Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, California, USA;Department of Obstetrics and Gynecology Städtische Klinikum Bielefeld (Academic Teaching Hospital University of Münster), Bielefeld, Germany;Department of Otorhinolaryngology, Head and Neck Surgery Klinikum Bielefeld (Academic Teaching Hospital University of Münster), Bielefeld, Germany;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;

关键词: Otitis Medium;    Acute Otitis Medium;    TUNEL Label;    Mucosal Hyperplasia;    Nontypeable Haemophilus Influenzae;   

DOI  :  10.1186/1471-2172-12-12

 received in 2010-11-02, accepted in 2011-01-26,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundTumor 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.ResultsTNFs 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.ConclusionsThe 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.

【 授权许可】

Unknown   
© Ebmeyer et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.