HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (Papers in Press[PDF]) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Stol, K. Articles by Hermans, P. W.M. PubMed PubMed Citation Articles by Stol, K. Articles by Hermans, P. W.M. Agricola Articles by Stol, K. Articles by Hermans, P. W.M.

Development of a non-invasive murine infection model for acute otitis media

¹ Department of Pediatrics, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands;
² Department of Pathology, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands;
³ Department of Otorhinolaryngology, Donders Institute for Brain, Cognition and Behaviour, Radboud Un

Otitis Media (OM) is one of the most frequent diseases in childhood, and Streptococcus pneumoniae is among the main causative bacterial agents. Since current experimental models used to study the bacterial pathogenesis of OM have several limitations, such as the invasiveness of the experimental procedures, we developed a non-invasive murine OM model. In our model, a pressure cabin is used in which a 40kPa pressure increase is applied to translocate pneumococci from the nasopharyngeal cavity into both mouse middle ears. This model was adapted from a previously developed rat OM model. Wild-type pneumococci were found to persist in the middle ear cavity for 144 hours after infection, with a maximum bacterial load at 96 hours. Inflammation was confirmed at 96 and 144 hours post infection by IL-1β and TNF- cytokine analysis and histopathology. Subsequently, we investigated the contribution of two surface-associated pneumococcal proteins, the streptococcal lipoprotein rotamase A (SlrA) and the putative proteinase maturation protein A (PpmA) to experimental OM in our model. Pneumococci lacking the gene encoding SlrA, but not PpmA were significantly reduced in virulence in the otitis media model. Importantly, pneumococci lacking both genes were significantly more attenuated than the slrA single mutant. This additive effect suggests that SlrA and PpmA exert complementary functions during experimental OM. In conclusion, we have developed a highly reproducible and non-invasive murine infection model for pneumococcal OM using a pressure cabin, which is very suitable to study pneumococcal pathogenesis and virulence in vivo.

⁴ E-mail: p.hermans{at}cukz.umcn.nl