Impaired T Helper 2 Response to Aeroallergen in Helminth‐Infected Patients with Asthma
Author(s) -
Maria Ilma Andrade Santos Araujo,
Bradford S. Hoppe,
Manoel Medeiros,
Luíz Carlos Júnior Alcântara,
Maria Cecília Almeida,
Albert Schriefer,
Ricardo Riccio Oliveira,
Ramon de Almeida Kruschewsky,
Joanemile P. Figueiredo,
Ãlvaro A. Cruz,
Edgar M. Carvalho
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/425017
Subject(s) - immunology , asthma , aeroallergen , peripheral blood mononuclear cell , allergy , schistosoma mansoni , medicine , helminths , immune system , helminthiasis , immunoglobulin e , schistosomiasis , allergen , biology , in vitro , antibody , biochemistry
Helminthic infections have been shown to inhibit allergy skin-prick tests and to modify the course of asthma. We evaluated Dermatophagoides pteronyssinus-specific immune responses in patients with asthma by measuring levels of T helper 2 (Th2) cytokines in peripheral blood mononuclear cell (PBMC) cultures. PBMCs from Schistosoma mansoni-infected patients with asthma living in an area of polyhelminthic endemicity produced lower levels of interleukin (IL)-5 and IL-4 in response to D. pteronyssinus antigen (Ag) 1 than did PBMCs from helminth-free patients with asthma. In contrast, D. pteronyssinus Ag 1-specific production of IL-10 was higher in helminth-infected patients than in helminth-free patients. The addition of recombinant human IL-10 to D. pteronyssinus Ag 1-stimulated cultures of PBMCs from helminth-free patients led to down-modulation of production of IL-5. After helminth-infected patients with asthma received antihelminthic treatment, there was down-modulation of D. pteronyssinus Ag 1-specific production of IL-10 in vitro. S. mansoni-infected patients with asthma produce lower levels of Th2 cytokines than do helminth-free patients with asthma, and this modulation is likely done by IL-10.
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