title: Neonatal immune responses to microbial stimuli: is there an influence of maternal allergy?
abstract: BACKGROUND
  Environmental factors are believed to play a role in the development of atopic allergy. This is likely to be important very early in life, at the fetal stage. The in utero environment could be affected by maternal allergy and in turn could influence the immune system of the baby.
  
  
  OBJECTIVE
  To investigate how cord blood mononuclear blood cells (CBMCs) from children of women with and without allergy respond to microbial stimuli.
  
  
  METHODS
  PBMCs from women with (n = 9) and without allergy (n = 10) and CBMCs from their newborn babies were stimulated in vitro with LPS and peptidoglycan. Cells were analyzed with flow cytometry for expression of CD14, Toll-like receptor (TLR)-2, and TLR4. The release of cytokines and chemokines (IL-1beta, IL-6, IL-8, IL-10, IL-12p70, TNF-alpha) and soluble CD14 into culture supernatants was measured with Cytometric Bead Array and ELISA, respectively.
  
  
  RESULTS
  Cord blood (CB) monocytes from children with mothers with allergy had significantly lower expression of TLR2 and TLR4 compared with maternal monocytes both before and after microbial stimulation, in contrast with CB monocytes from children with mothers without allergy. Further, CBMCs from children with mothers with allergy had a lower ( P = .03) IL-6 response after stimulation with peptidoglycan than CBMCs from children with mothers without allergy.
  
  
  CONCLUSIONS
  Our results imply that CB monocytes and CBMC immune responses are influenced by maternal allergy. On the basis of these findings, we speculate that monocytes from children with mothers with allergy have a reduced capacity to respond to microbial stimuli.
authors.affiliation: Department of Immunology, Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Petra
authors.initials: P
authors.lastname: Amoudruz
authors.forename: Ulrika
authors.initials: U
authors.lastname: Holmlund
authors.forename: Vivianne
authors.initials: V
authors.lastname: Malmström
authors.forename: Christina
authors.initials: C
authors.lastname: Trollmo
authors.forename: Katarina
authors.initials: K
authors.lastname: Bremme
authors.forename: Annika
authors.initials: A
authors.lastname: Scheynius
authors.forename: Eva
authors.initials: E
authors.lastname: Sverremark-Ekström
mesh_terms: D000328:Adult; D002478:Cells, Cultured; D005260:Female; D005312:Fetal Blood; D006801:Humans; D006967:Hypersensitivity / Q000097:blood / Q000150:complications* / Q000276:immunology; D015850:Interleukin-6 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis; D008070:Lipopolysaccharides; D008297:Male; D018811:Maternal Exposure; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D010457:Peptidoglycan; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000276:immunology*; D011956:Receptors, Cell Surface / Q000096:biosynthesis; D012307:Risk Factors; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors
chemical_list: D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D010457:Peptidoglycan; D011956:Receptors, Cell Surface; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors