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TLR3 in Human Eosinophils: Functional Effects and Decreased Expression during Allergic Rhinitis.

Månsson, Anne LU ; Fransson, Mattias LU ; Adner, Mikael LU ; Benson, Mikael ; Uddman, Rolf LU ; Björnsson, Sven LU and Cardell, Lars-Olaf LU (2010) In International Archives of Allergy and Immunology 151(2). p.118-128
Abstract
Background/Aim: Viral respiratory infections are increasingly implicated in allergic exacerbations. Virus-induced activation of eosinophils through Toll-like receptors (TLRs) could be involved. The present study was designed to examine TLR3 expression in eosinophils from bone marrow (BM) and peripheral blood (PB) during symptomatic allergic rhinitis, and to evaluate the functional responsiveness of TLR3 in purified eosinophils. Methods: BM and PB samples were obtained from healthy volunteers and patients with seasonal allergic rhinitis outside and during the pollen season. Eosinophils were analyzed for TLR3 expression by flow cytometry. Polyinosinic:polycytidylic acid [poly(I:C)], an agonist for TLR3, was used to assess its functional role... (More)
Background/Aim: Viral respiratory infections are increasingly implicated in allergic exacerbations. Virus-induced activation of eosinophils through Toll-like receptors (TLRs) could be involved. The present study was designed to examine TLR3 expression in eosinophils from bone marrow (BM) and peripheral blood (PB) during symptomatic allergic rhinitis, and to evaluate the functional responsiveness of TLR3 in purified eosinophils. Methods: BM and PB samples were obtained from healthy volunteers and patients with seasonal allergic rhinitis outside and during the pollen season. Eosinophils were analyzed for TLR3 expression by flow cytometry. Polyinosinic:polycytidylic acid [poly(I:C)], an agonist for TLR3, was used to assess its functional role in purified eosinophils and the intracellular signaling pathways involved. Results: TLR3 expression was demonstrated in BM and PB eosinophils. It was higher in BM-derived than in circulating cells and it was downregulated in both compartments during symptomatic allergic rhinitis. TLR3 expression was also downregulated in the presence of interleukin (IL)-4 and IL- 5. Stimulation with poly(I:C) increased the percentage of CD11b+ cells and enhanced the secretion of IL-8, effects mediated via the p38 mitogen-activated protein kinases and nuclear factor-kappaB signaling pathways. Moreover, pretreatment with IL-5 augmented the poly(I:C)-induced IL-8 release. Conclusions: Eosinophils activated via TLR3 might be more able to home and recruit leukocytes to sites of inflammation. The decreased TLR3 expression during symptomatic allergic rhinitis and in the presence of Th2 cytokines indicates a role in allergic airway inflammation. Thus, eosinophils might function as a link between viral infections and exacerbations of allergic disease. (Less)
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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
International Archives of Allergy and Immunology
volume
151
issue
2
pages
118 - 128
publisher
Karger
external identifiers
  • wos:000269790700004
  • pmid:19752565
  • scopus:70049117774
  • pmid:19752565
ISSN
1423-0097
DOI
10.1159/000236001
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Clinical and Experimental Allergy Research (013243510), Reconstructive Surgery (013240300), Clinical Chemistry, Malmö (013016000)
id
c1f45bed-9934-4cca-b3ca-12ef7a5b119c (old id 1483517)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19752565?dopt=Abstract
date added to LUP
2016-04-04 07:10:14
date last changed
2022-03-15 06:31:23
@article{c1f45bed-9934-4cca-b3ca-12ef7a5b119c,
  abstract     = {{Background/Aim: Viral respiratory infections are increasingly implicated in allergic exacerbations. Virus-induced activation of eosinophils through Toll-like receptors (TLRs) could be involved. The present study was designed to examine TLR3 expression in eosinophils from bone marrow (BM) and peripheral blood (PB) during symptomatic allergic rhinitis, and to evaluate the functional responsiveness of TLR3 in purified eosinophils. Methods: BM and PB samples were obtained from healthy volunteers and patients with seasonal allergic rhinitis outside and during the pollen season. Eosinophils were analyzed for TLR3 expression by flow cytometry. Polyinosinic:polycytidylic acid [poly(I:C)], an agonist for TLR3, was used to assess its functional role in purified eosinophils and the intracellular signaling pathways involved. Results: TLR3 expression was demonstrated in BM and PB eosinophils. It was higher in BM-derived than in circulating cells and it was downregulated in both compartments during symptomatic allergic rhinitis. TLR3 expression was also downregulated in the presence of interleukin (IL)-4 and IL- 5. Stimulation with poly(I:C) increased the percentage of CD11b+ cells and enhanced the secretion of IL-8, effects mediated via the p38 mitogen-activated protein kinases and nuclear factor-kappaB signaling pathways. Moreover, pretreatment with IL-5 augmented the poly(I:C)-induced IL-8 release. Conclusions: Eosinophils activated via TLR3 might be more able to home and recruit leukocytes to sites of inflammation. The decreased TLR3 expression during symptomatic allergic rhinitis and in the presence of Th2 cytokines indicates a role in allergic airway inflammation. Thus, eosinophils might function as a link between viral infections and exacerbations of allergic disease.}},
  author       = {{Månsson, Anne and Fransson, Mattias and Adner, Mikael and Benson, Mikael and Uddman, Rolf and Björnsson, Sven and Cardell, Lars-Olaf}},
  issn         = {{1423-0097}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{118--128}},
  publisher    = {{Karger}},
  series       = {{International Archives of Allergy and Immunology}},
  title        = {{TLR3 in Human Eosinophils: Functional Effects and Decreased Expression during Allergic Rhinitis.}},
  url          = {{http://dx.doi.org/10.1159/000236001}},
  doi          = {{10.1159/000236001}},
  volume       = {{151}},
  year         = {{2010}},
}