title: Developmental changes in interleukin-12-producing ability by monocytes and their relevance to allergic diseases.
abstract: BACKGROUND
  The T helper type-2 (Th2)-dominated situation can be observed in allergic diseases such as asthma or atopic dermatitis. A reduced ability to produce IL-12, which is a key cytokine for the induction of Th1 responses, has been proposed to lead to aberrant Th2 development in these disease conditions.
  
  
  OBJECTIVE
  This study was intended to examine how IL-12-producing ability might associate with allergic diseases as a function of age.
  
  
  METHODS
  IL-12 production by monocytes at various ages was assessed in patients with bronchial asthma and/or atopic dermatitis (n = 100) in comparison with non-allergic control subjects (n = 144). Whole blood cells were stimulated with lipopolysaccharide (LPS) after priming with IFN-gamma, then intracellular cytokine expression of IL-12 and IL-8 as a control cytokine of CD14-positive cells was assessed by flow cytometric analysis.
  
  
  RESULTS
  In the control subjects, the ability of monocytes to produce IL-12 was negligible at birth and gradually increased with advancing age, whereas IL-8 production was intense throughout the human life. At more than 7 years of age, IL-12 production of patients with allergic diseases was significantly lower compared with that of control subjects. The unexpected finding was that infants and children below 6 years of age with allergic diseases tended to produce more IL-12 compared with age-matched controls. In this young group, it was noted that enhanced IL-12 production by monocytes was especially observed in allergic patients with specific IgE antibodies against some food allergens. Significant inverse relationships between serum IgE levels and IL-12-producing ability were found in the teenage and adult groups, but not in the younger children.
  
  
  CONCLUSIONS
  IL-12 appeared to play different roles in the pathogenesis of allergic diseases between younger and older ages.
authors.affiliation: Department of Pediatrics, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Itazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Adachi
authors.forename: Y
authors.initials: Y
authors.lastname: Okabe
authors.forename: M
authors.initials: M
authors.lastname: Hamamichi
authors.forename: Y S
authors.initials: YS
authors.lastname: Adachi
authors.forename: M
authors.initials: M
authors.lastname: Toyoda
authors.forename: M
authors.initials: M
authors.lastname: Morohashi
authors.forename: T
authors.initials: T
authors.lastname: Miyawaki
mesh_terms: D000293:Adolescent; D000328:Adult; D000375:Aging / Q000276:immunology*; D001249:Asthma / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000276:immunology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007223:Infant; D007231:Infant, Newborn; D007371:Interferon-gamma / Q000494:pharmacology; D018664:Interleukin-12 / Q000096:biosynthesis*; D016209:Interleukin-8 / Q000096:biosynthesis; D018950:Lipopolysaccharide Receptors / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D013601:T-Lymphocytes / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D016209:Interleukin-8; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D018664:Interleukin-12; D007371:Interferon-gamma