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Originally published online as doi:10.1189/jlb.0709518 on October 20, 2009

Published online before print October 20, 2009
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(Journal of Leukocyte Biology. 2010;87:213-222.)
© 2010 The Author(s)

Immunopathogenesis of polymicrobial otitis media

Lauren O. Bakaletz1

The Research Institute at Nationwide Children’s Hospital, Center for Microbial Pathogenesis, The Ohio State University College of Medicine, Columbus, Ohio, USA

1. Correspondence: Center for Microbial Pathogenesis, The Research Institute at Nationwide Children’s Hospital, Rm. W591, The Ohio State University College of Medicine, 700 Children’s Dr., Columbus, OH 43205-2696, USA. E-mail: lauren.bakaletz{at}nationwidechildrens.org

OM, or inflammation of the middle ear, is a highly prevalent infection in children worldwide. OM is a multifactorial disease with multiple risk factors, including preceding or concurrent viral URT infection. Hence, OM is also a polymicrobial disease. The mechanisms by which viruses predispose to bacterial OM are replete; however, all are predicated on the general principle of compromise of primary host airway defenses. Thus, despite an as-yet incomplete understanding of the molecular mechanisms involved in bacterial superinfection of a virus-compromised respiratory tract, the URT viruses are known to induce histopathology of airway mucosal epithelium, up-regulate expression of eukaryotic receptors used for bacterial adherence, alter the biochemical and rheological properties of airway mucus, and affect innate and acquired host immune functions, among others. Although discussed here in the context of OM, during preceding or concurrent viral infection of the human respiratory tract, viral impairment of airway defenses and the resulting predisposition to subsequent bacterial coinfection are also known to be operational in the mid and lower airway as well.

Key Words: ear infection • innate immunity • nontypeable Haemophilus influenzaeStreptococcus pneumoniaeMoraxella catarrhalis • Eustachian tube