title: TLR2 promotes macrophage recruitment and Streptococcus pneumoniae clearance during mouse otitis media.
abstract: The natural course of otitis media (OM) in most children is acute and self-limiting; however, approximately 10-20% of children can experience persistent or recurrent OM. Determining the host factors that influence outcome of OM will help us design better therapies. This study focused on the role of Toll-like receptor 2 (TLR2) in a pneumococcal OM mouse model.
  
  
  
  The middle ears (MEs) of wild-type (WT) and TLR2-/-mice were inoculated with Streptococcus pneumoniae (Spn) serotype 19F via transbullar injection. ME TLR2 expression in WT mice was determined by qRT-PCR and immunofluorescence. ME pathological manifestations, inflammatory response, and pneumococcal clearance between WT and TLR2-/-mice were compared after Spn inoculation.
  
  
  
  TLR2 expression in ME mucosa was markedly enhanced following infection with Spn in WT mice. In contrast to WT mice, TLR2-/-mice exhibited unaffected early ME inflammatory response. During late stage of ME infection, however, the absence of TLR2 can lead to reduced macrophage recruitment, impaired Spn clearance, and prolonged ME inflammation.
  
  
  
  Our results demonstrate that TLR2 signaling is critical for bacterial clearance and timely resolution of inflammation in OM induced by Spn.
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.|Department of Laboratory Medicine, Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, China.
authors.forename: Yifei
authors.initials: Y
authors.lastname: Huang
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Zimeng
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Chunfang
authors.initials: C
authors.lastname: Jin
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Xuemei
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Wenchun
authors.initials: W
authors.lastname: Xu
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Xiang
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.affiliation: Department of Laboratory Medicine, Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, China.
authors.forename: Xiujing
authors.initials: X
authors.lastname: He
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Yibing
authors.initials: Y
authors.lastname: Yin
authors.affiliation: Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Yujuan
authors.initials: Y
authors.lastname: He
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004432:Ear, Middle / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010033:Otitis Media / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D011008:Pneumococcal Infections / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D013296:Streptococcus pneumoniae / Q000145:classification / Q000302:isolation & purification; D051195:Toll-Like Receptor 2 / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D057170:Translational Research, Biomedical; D015854:Up-Regulation
chemical_list: C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2