title: Cord blood cytokines and chemokines and development of allergic disease.
abstract: Exposure to ubiquitous allergens early in life, even before birth, may influence the incidence of allergic diseases later in life. During pregnancy, the fetomaternal interface is surrounded by high levels of T-helper (Th)2-like cytokines, possibly favouring the development of Th2-like immune responses in the offspring. The aim of this study was to evaluate the relation between cord blood (CB) IgE antibodies, Th1- and Th2-like cytokines and chemokines, maternal allergy and development of allergic disease during the first 2 yr of life in the offspring. The CB cytokine and chemokine levels from children of 20 allergic and 36 non-allergic women were determined by a multiplexed Luminex assay and ELISA. Total CB and maternal IgE antibody concentrations were quantified using ImmunoCAP technology. The maternal IgE levels during and after pregnancy correlated with CB IgE and Th2-associated macrophage-derived chemokine [MDC (CCL22)] levels. Development of allergic disease and sensitization was associated with increased CB IgE and MDC (CCL22) levels, as well as high ratios of MDC (CCL22) to Th1-associated interferon-gamma inducible protein 10 [IP-10 (CXCL10)] and interferon-gamma inducible T-cell alpha-chemoattractant [I-TAC (CXCL11) (n = 7 allergic vs. n = 25 non-allergic)]. The correlations between maternal IgE and CB IgE and MDC (CCL22) levels possibly indicate that the maternal immunity can affect the Th1/Th2 profile in the neonate. Development of allergic disease is associated with a more marked Th2-like deviation already at birth, shown as increased levels of CB IgE and MDC (CCL22) and higher ratios of MDC (CCL22) to IP-10 (CXCL10) and I-TAC (CXCL11).
authors.affiliation: Division of Pediatrics, Department of Clinical and Experimental Medicine, Clinical Research Centre, Faculty of Health Sciences, Linköping University, SE-581 85 Linköping, Sweden. marsa@imk.liu.se
authors.forename: Martina
authors.initials: M
authors.lastname: Sandberg
authors.forename: Anne
authors.initials: A
authors.lastname: Frykman
authors.forename: Jan
authors.initials: J
authors.lastname: Ernerudh
authors.forename: Göran
authors.initials: G
authors.lastname: Berg
authors.forename: Leif
authors.initials: L
authors.lastname: Matthiesen
authors.forename: Christina
authors.initials: C
authors.lastname: Ekerfelt
authors.forename: Lennart J
authors.initials: LJ
authors.lastname: Nilsson
authors.forename: Maria C
authors.initials: MC
authors.lastname: Jenmalm
mesh_terms: D000328:Adult; D001249:Asthma / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism; D054422:Chemokine CCL22 / Q000097:blood; D054357:Chemokine CXCL10 / Q000097:blood; D054371:Chemokine CXCL11 / Q000097:blood; D018925:Chemokines / Q000097:blood; D002675:Child, Preschool; D003231:Conjunctivitis / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000097:blood*; D005260:Female; D005312:Fetal Blood / Q000276:immunology / Q000378:metabolism; D005865:Gestational Age; D006801:Humans; D006967:Hypersensitivity / Q000175:diagnosis / Q000276:immunology* / Q000378:metabolism; D007073:Immunoglobulin E / Q000097:blood; D007223:Infant; D008297:Male; D011247:Pregnancy; D012220:Rhinitis / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism; D055815:Young Adult
chemical_list: C515482:CCL22 protein, human; D054422:Chemokine CCL22; D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D018925:Chemokines; D016207:Cytokines; D007073:Immunoglobulin E