title: Lower expression of TLR2 and SOCS-3 is associated with Schistosoma haematobium infection and with lower risk for allergic reactivity in children living in a rural area in Ghana.
abstract: BACKGROUND
  Helminth infections are prevalent in rural areas of developing countries and have in some studies been negatively associated with allergic disorders and atopy. In this context little is known of the molecular mechanisms of modulation involved. We have characterized the innate immune responses, at the molecular level, in children according to their helminth infection status and their atopic reactivity to allergens.
  
  
  RESULTS
  The mRNA expression of several genes of the innate immune system that have been associated with microbial exposure and allergy was examined in 120 school children in a rural area in Ghana. Helminth infections were common and atopy rare in the study area. The analysis of gene expression in ex vivo whole blood samples reflected the levels of corresponding proteins. Using this approach in a population of school children in whom the presence of Schistosoma haematobium infection was associated with protection from atopic reactivity, we found that the level of TLR2 and SOCS-3, genes associated with atopy in the children, were significantly downregulated by presence of S. haematobium infection.
  
  
  CONCLUSIONS
  S. haematobium infections modulate the expression of genes of the innate immune system (TLR2 and SOCS-3); these are genes that are associated with increased allergic inflammatory processes, providing a molecular link between the negative association of this infection and atopy in rural children in Ghana.
authors.affiliation: Department of Parasitology, Leiden University Medical Centre, Leiden, The Netherlands. F.C.Hartgers@lumc.nl
authors.forename: Franca C
authors.initials: FC
authors.lastname: Hartgers
authors.forename: Benedicta B
authors.initials: BB
authors.lastname: Obeng
authors.forename: Yvonne C M
authors.initials: YC
authors.lastname: Kruize
authors.forename: Marjolijn
authors.initials: M
authors.lastname: Duijvestein
authors.forename: Anna
authors.initials: A
authors.lastname: de Breij
authors.forename: Abena
authors.initials: A
authors.lastname: Amoah
authors.forename: Irene A
authors.initials: IA
authors.lastname: Larbi
authors.forename: Ronald
authors.initials: R
authors.lastname: van Ree
authors.forename: Michael D
authors.initials: MD
authors.lastname: Wilson
authors.forename: Laura C
authors.initials: LC
authors.lastname: Rodrigues
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Boakye
authors.forename: Maria
authors.initials: M
authors.lastname: Yazdanbakhsh
mesh_terms: D000818:Animals; D002648:Child; D002675:Child, Preschool; D005260:Female; D005434:Flow Cytometry; D005869:Ghana / Q000453:epidemiology; D006801:Humans; D006967:Hypersensitivity / Q000097:blood / Q000276:immunology*; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D016133:Polymerase Chain Reaction; D039981:Pyroglyphidae / Q000276:immunology*; D012553:Schistosomiasis haematobia / Q000453:epidemiology / Q000235:genetics / Q000276:immunology*; D012867:Skin / Q000276:immunology; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics*
chemical_list: C108944:SOCS1 protein, human; C106644:SOCS3 protein, human; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D007073:Immunoglobulin E