13 research outputs found
Summary of ‘Antihistamines and/or decongestants for otitis media with effusion (OME) in children’
Antibiotics for simple upper respiratory tract infections: a survey of academic, pediatric, and adult clinical allergists
One-stage coclear implantation via a facial recess approach in children with otitis media with effusion
Comparative Profile of Heme Acquisition Genes in Disease-Causing and Colonizing Nontypeable Haemophilus influenzae and Haemophilus haemolyticus
Commentary on ‘Antihistamines and/or decongestants for otitis media with effusion (OME) in children’, with a reply from the review author
NTHi induction of Cxcl2 and middle ear mucosal metaplasia in mice
OBJECTIVE: Chronic Otitis Media (COM) develops after sustained inflammation and is characterized by secretory middle ear epithelial metaplasia and effusion, most frequently mucoid. Non-typeable Haemophilus influenzae (NTHi), the most common acute OM pathogen, is known to activate inflammation and mucin expression in vitro and in animal models of OM. The goals of this study were to examine histopathological and expression profiling epithelial effects of NTHi challenge in murine middle ears. STUDY DESIGN: In vitro and in vivo murine model of OM. METHODS: Weekly transtympanic inoculation of Balb/c mice with 300 μg/ml of NTHi lysates vs saline was performed. Histopathologic analysis was carried out at 4 weeks. Expression microarray analysis was performed at 1 and 7 days. Microarray findings were validated in independent animal samples and in a cultured murine middle ear epithelial cell (mMEEC) line. RESULTS: Histopathologic analyses revealed middle ear mucosal thickening after NTHi exposure. Microarray analyses of inflammatory response genes that changed significantly demonstrated that the chemokine Cxcl2 had the largest fold-change with significantly increased expression at 1 and 7 days after NTHi injection compared to either saline or no-injection (p<0.01). Validation by realtime qPCR revealed similar significantly increased relative mRNA levels for Cxcl2. NTHi lysates were also found to significantly up-regulate the transcription of Cxcl2 in mMEEC in a time and dose dependent manner (p<0.05). CONCLUSIONS: Middle ear NTHi challenge in mice leads to chronic epithelial mucosal metaplasia and over-expression of inflammatory mediators, most notably Cxcl2. This finding is parallel to NTHi mediated pulmonary mucosal metaplasia where Cxcl2 has been identified as an important inflammatory mediator