title: The effect of peptidoglycan stimulation on basophil-mediated atopic responses during pregnancy and in newborns.
abstract: BACKGROUND
  Toll-like receptor (TLR) molecules play critical roles in directing the course of atopic diseases by recognizing specific microbial products that activate immune effector cell function.
  
  
  OBJECTIVE
  We determined if basophils harvested from neonates genetically predisposed to atopic disease had different levels of TLR2 expression and determined whether putative TLR2 ligands mediated cytokine secretion.
  
  
  METHODS
  Blood samples were collected from 10 asthmatic and 12 healthy women and their newborns. Basophil histamine was measured using the human basophil degranulation test and TLR2 expression was determined using nucleic acid hybridization in situ and flow cytometry. IL-4 levels were quantified by ELISA following allergen stimulation.
  
  
  RESULTS
  The basophil degranulation index (DI) in granulocytes harvested from peripheral blood of asthmatic women was assessed following stimulation with either peptidoglycan (PGN) or Dermatophagoides farinae (Df) extract. The DI was significantly higher in atopic women than in healthy controls. Basophils purified from the cord blood of neonates born to atopic mothers produced more IL-4 compared with basophils purified from children born to nonatopic controls. Finally, TLR2 expression at the protein and mRNA levels was upregulated in cord blood basophils from neonates born to mothers with asthma following stimulation with PGN but not Df.
  
  
  CONCLUSIONS
  These data suggested that TLR2-mediated innate immune responses play a role in augmenting allergic reactions through the modulation of basophil cytokine secretion and histamine release. Microbial components may activate basophils through TLR2 (especially for genetically predisposed infants) to release cytokines associated with an increased incidence of allergic diseases.
authors: Department of Geriatrics, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
authors: Ling
authors: L
authors: Yang
authors: Wei-Guo
authors: WG
authors: Xu
authors: Yi-Ping
authors: YP
authors: Xu
authors: Yin-Shi
authors: YS
authors: Guo
authors: Ying
authors: Y
authors: Xiong
authors: Gui-Ying
authors: GY
authors: Shi
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D015549:Basophil Degranulation Test; D001491:Basophils / Q000187:drug effects / Q000276:immunology* / Q000502:physiology; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D005312:Fetal Blood / Q000166:cytology; D020022:Genetic Predisposition to Disease; D006636:Histamine Release; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics / Q000276:immunology*; D007113:Immunity, Innate; D007223:Infant; D007231:Infant, Newborn / Q000276:immunology* / Q000378:metabolism; D015847:Interleukin-4 / Q000096:biosynthesis; D008024:Ligands; D010457:Peptidoglycan / Q000008:administration & dosage*; D049590:Postpartum Period / Q000276:immunology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism*
chemical_list: D016207:Cytokines; D008024:Ligands; D010457:Peptidoglycan; D012333:RNA, Messenger; C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2; D015847:Interleukin-4