Hypoallergenic fragment of Par j 2 increases functional expression of Toll‐like receptors in atopic children

Background:  Parietaria judaica (Par j) is one of the main causes of allergy in the Mediterranean countries. The activation of Toll‐like receptor 4 (TLR4) by lipopolysaccharide (LPS) inhibits nasal inflammation of atopic children. Objective:  To examine, in vivo and in vitro, the effect of recombina...

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Veröffentlicht in:Allergy (Copenhagen) 2006-12, Vol.61 (12), p.1459-1466
Hauptverfasser: Pace, E., Duro, G., Grutta, S. La, Ferraro, M., Bruno, A., Bousquet, J., Bonsignore, G., Gjomarkaj, M.
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Sprache:eng
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Zusammenfassung:Background:  Parietaria judaica (Par j) is one of the main causes of allergy in the Mediterranean countries. The activation of Toll‐like receptor 4 (TLR4) by lipopolysaccharide (LPS) inhibits nasal inflammation of atopic children. Objective:  To examine, in vivo and in vitro, the effect of recombinant Par j 2 (rPar j 2) and of its fragments (1–55 and 52–102) on atopic children. Methods:  We used skin prick test for in vivo evaluations. We assessed, in vitro, in peripheral blood mononuclear cells (PBMC), the effect of rPar j 2 and of the two fragments on neutrophil chemotaxis, on CD45RO, on TLR2 and TLR4 expression, on LPS binding and on interferon (IFN)‐γ release, by a microchemotaxis chamber, by flow cytometry and by enzyme‐linked immunosorbent assay, respectively. Results:  In vivo while rPar j 2 induced a positive skin reaction, 1–55 and 52–102 fragments did not. In vitro, while rPar j 2 increased both CD45RO expression and neutrophils chemotaxis in PBMC, both Par j 2 fragments did not. 1–55 fragment of Par j 2 upregulated both TLR2 and TLR4 expression and LPS binding, while the rPar j 2 and 52–102 fragment did not. Finally, 1–55 fragment of Par j 2 induced IFNγ release, while the rPar j 2 and 52–102 fragment did not. Conclusions:  Hypoallergenic 1–55 fragment, upregulating innate immunity receptors and increasing IFNγ, might re‐orientate, in atopics, the immune system toward a physiologic balance between Th1 and Th2 responses.
ISSN:0105-4538
1398-9995
DOI:10.1111/j.1398-9995.2006.01234.x