title: Infant home endotoxin is associated with reduced allergen-stimulated lymphocyte proliferation and IL-13 production in childhood.
abstract: BACKGROUND
  Infant endotoxin exposure has been proposed as a factor that might protect against allergy and the early childhood immune responses that increase the risk of IgE production to allergens.
  
  
  OBJECTIVE
  Using a prospective study design, we tested the hypothesis that early-life endotoxin exposure is associated with allergen- and mitogen-induced cytokine production and proliferative responses of PBMCs isolated from infants with a parental history of physician-diagnosed asthma or allergy.
  
  
  METHODS
  We assessed household dust endotoxin at age 2 to 3 months and PBMC proliferative and cytokine responses to cockroach allergen (Bla g 2), dust mite allergen (Der f 1), cat allergen (Fel d 1), and the nonspecific mitogen PHA at age 2 to 3 years.
  
  
  RESULTS
  We found that increased endotoxin levels were associated with decreased IL-13 levels in response to cockroach, dust mite, and cat allergens, but not mitogen stimulation. Endotoxin levels were not correlated with allergen- or mitogen-induced IFN-gamma, TNF-alpha, or IL-10. Increased endotoxin levels were associated with decreased lymphocyte proliferation after cockroach allergen stimulation. An inverse, although nonsignificant, association was also found between endotoxin and proliferation to the other tested stimuli.
  
  
  CONCLUSIONS
  Increased early-life exposure to household endotoxin was associated with reduced allergen-induced production of the TH2 cytokine IL-13 and reduced lymphoproliferative responses at age 2 to 3 years in children at risk for allergy and asthma. Early-life endotoxin-related reduction of IL-13 production might represent one pathway through which increased endotoxin decreases the risk of allergic disease and allergy in later childhood.
authors.affiliation: Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
authors.forename: Joseph H
authors.initials: JH
authors.lastname: Abraham
authors.forename: Patricia W
authors.initials: PW
authors.lastname: Finn
authors.forename: Donald K
authors.initials: DK
authors.lastname: Milton
authors.forename: Louise M
authors.initials: LM
authors.lastname: Ryan
authors.forename: David L
authors.initials: DL
authors.lastname: Perkins
authors.forename: Diane R
authors.initials: DR
authors.lastname: Gold
mesh_terms: D000485:Allergens / Q000276:immunology*; D002675:Child, Preschool; D004391:Dust / Q000032:analysis; D004731:Endotoxins / Q000494:pharmacology*; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000517:prevention & control*; D007223:Infant; D018793:Interleukin-13 / Q000096:biosynthesis*; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000502:physiology; D011446:Prospective Studies; D011956:Receptors, Cell Surface / Q000502:physiology; D051193:Toll-Like Receptors
chemical_list: D000485:Allergens; D004391:Dust; D004731:Endotoxins; D018793:Interleukin-13; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors