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  • 1
    Electronic Resource
    Electronic Resource
    Developmental changes in interleukin-12-producing ability by monocytes and their relevance to allergic diseases (2003)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 33 (2003), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 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-γ, 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.Conclusion IL-12 appeared to play different roles in the pathogenesis of allergic diseases between younger and older ages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2003.01608.x
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  • 2
    Electronic Resource
    Electronic Resource
    Increased lymphoid MxA expression in acute asthma exacerbation in children (2001)
    Copenhagen : Munksgaard International Publishers
    Allergy 56 (2001), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Although the association between acute asthma exacerbation and viral infection has been well documented, virus identification rates vary. It has recently been reported that the expression of MxA protein in lymphocytes, inducible by type I interferons, can serve as a sensitive marker for viral infection in the host. The objective was to determine the contribution of viral infection to precipitation of asthma attacks in children. Methods: We studied 186 asthmatic children, aged 0–12 years, over a 1-year period to evaluate MxA protein levels in peripheral blood lymphocytes by using a flow cytometric analysis in whole blood. Results: Of all the subjects, 80 (47%) exhibited significantly elevated levels of MxA expression in lymphocytes, presumably indicating the states of viral infection. The association of viral infections with acute asthma exacerbation seemed to be marked in younger children: enhanced MxA expression was seen in 73.3% of infants (aged 0–1 year), 49.5% of toddlers (aged 2–5 years), and 26% of schoolchildren (aged 6–12 years). Seasonal changes in the frequency of viral infection associated with deterioration were also observed. Conclusions: Flow cytometric assay of MxA protein expression in whole blood appears to be an easy and useful method to evaluate viral infections in acute asthma exacerbation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.2001.00312.x
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    Paper (German National Licenses)
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