title: Differences in innate immune response gene regulation in the middle ear of children who are otitis prone and in those not otitis prone.
abstract: OBJECTIVE
  Acute otitis media (AOM) causes an inflammatory response in the middle ear. We assessed differences in innate immune responses involved in bacterial defense at onset of AOM in children who were stringently defined as otitis prone (sOP) and children not otitis prone (NOP).
  
  
  METHODS
  Innate immune genes analysis from middle ear fluid (MEF) samples of children.
  
  
  METHODS
  Genes of toll-like receptors (TLR), nod-like and retinoic acid-inducible gene-I-like receptors, downstream effectors important for inflammation and apoptosis, including cytokines and chemokines, were studied from MEF samples by using a real-time polymerase chain reaction array. Protein levels of differentially regulated genes were measured by Luminex.
  
  
  RESULTS
  Gene expression in MEF among children who were sOP was significantly different in upregulation of interleukin 8, secretory leukocyte peptidase inhibitor, and chemokine (C-C motif) ligand 3, and in downregulation of interferon regulatory factor 7 and its related signaling molecules interferon alpha, Toll-like receptor adaptor molecule 2, chemokine (C-C motif) ligand 5, and mitogen-activated protein kinase 8 compared with children who were NOP. Differences in innate gene regulation were similar when AOM was caused by Streptococcus pneumoniae or nontypeable Haemophilus influenzae.
  
  
  CONCLUSIONS
  Innate-immune response genes are differentially regulated in children who were sOP compared with children with NOP.
authors.affiliation: Center for Infectious Diseases and Immunology, Rochester General Hospital Research Institute, Rochester, New York, USA.
authors.forename: Ravinder
authors.initials: R
authors.lastname: Kaur
authors.forename: Janet
authors.initials: J
authors.lastname: Casey
authors.forename: Michael
authors.initials: M
authors.lastname: Pichichero
mesh_terms: D000293:Adolescent; D054405:Chemokine CCL3 / Q000235:genetics / Q000378:metabolism; D018946:Chemokine CCL5 / Q000235:genetics / Q000378:metabolism; D002648:Child; D004432:Ear, Middle / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D020022:Genetic Predisposition to Disease; D044135:Haemophilus parainfluenzae; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D050839:Interferon Regulatory Factor-7 / Q000235:genetics / Q000378:metabolism; D016898:Interferon-alpha / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008297:Male; D010033:Otitis Media / Q000235:genetics* / Q000276:immunology; D011446:Prospective Studies; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000235:genetics / Q000378:metabolism; D013296:Streptococcus pneumoniae; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism
chemical_list: C515429:CCL3 protein, human; D054405:Chemokine CCL3; D018946:Chemokine CCL5; C494234:IRF7 protein, human; D050839:Interferon Regulatory Factor-7; D016898:Interferon-alpha; D016209:Interleukin-8; D053481:Secretory Leukocyte Peptidase Inhibitor; C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2