Diminished levels of nasal S100A7 (psoriasin) in seasonal allergic rhinitis: an effect mediated by Th2 cytokines
(2012) In Respiratory Research 13.- Abstract
- Background: S100A7 is an antimicrobial peptide involved in several inflammatory diseases. The aim of the present study was to explore the expression and regulation of S100A7 in seasonal allergic rhinitis (SAR). Methods: Nasal lavage (NAL) fluid was obtained from healthy controls before and after lipopolysaccharide (LPS) provocation, from SAR patients before and after allergen challenge, and from SAR patients having completed allergen-specific immunotherapy (ASIT). Nasal biopsies, nasal epithelial cells and blood were acquired from healthy donors. The airway epithelial cell line FaDu was used for in vitro experiments. Real-time RT-PCR and immunohistochemistry were used to determine S100A7 expression in nasal tissue and cells. Release of... (More)
- Background: S100A7 is an antimicrobial peptide involved in several inflammatory diseases. The aim of the present study was to explore the expression and regulation of S100A7 in seasonal allergic rhinitis (SAR). Methods: Nasal lavage (NAL) fluid was obtained from healthy controls before and after lipopolysaccharide (LPS) provocation, from SAR patients before and after allergen challenge, and from SAR patients having completed allergen-specific immunotherapy (ASIT). Nasal biopsies, nasal epithelial cells and blood were acquired from healthy donors. The airway epithelial cell line FaDu was used for in vitro experiments. Real-time RT-PCR and immunohistochemistry were used to determine S100A7 expression in nasal tissue and cells. Release of S100A7 in NAL and culture supernatants was measured by ELISA. The function of recombinant S100A7 was explored in epithelial cells, neutrophils and peripheral blood mononuclear cells (PBMC). Results: Nasal administration of LPS induced S100A7 release in healthy non-allergic subjects. The level of S100A7 was lower in NAL from SAR patients than from healthy controls, and it was further reduced in the SAR group 6 h post allergen provocation. In contrast, ASIT patients displayed higher levels after completed treatment. S100A7 was expressed in the nasal epithelium and in glands, and it was secreted by cultured epithelial cells. Stimulation with IL-4 and histamine repressed the epithelial S100A7 release. Further, recombinant S100A7 induced activation of neutrophils and PBMC. Conclusions: The present study shows an epithelial expression and excretion of S100A7 in the nose after microbial stimulation. The levels are diminished in rhinitis patients and in the presence of an allergic cytokine milieu, suggesting that the antimicrobial defense is compromised in patients with SAR. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2515897
- author
- Kvarnhammar, Anne Mansson ; Rydberg, Camilla ; Jarnkrants, Malin ; Eriksson, Mia ; Uddman, Rolf LU ; Benson, Mikael and Cardell, Lars-Olaf
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Th2 cytokines, lipopolysaccharide, seasonal allergic rhinitis, antimicrobial peptide, epithelium, allergen-specific immunotherapy
- in
- Respiratory Research
- volume
- 13
- publisher
- BioMed Central (BMC)
- external identifiers
-
- wos:000301716000001
- scopus:84857457223
- pmid:22230654
- ISSN
- 1465-9921
- DOI
- 10.1186/1465-9921-13-2
- language
- English
- LU publication?
- yes
- id
- fc2a7749-008f-4922-a919-8697467b5177 (old id 2515897)
- date added to LUP
- 2016-04-01 10:43:37
- date last changed
- 2022-02-17 20:49:28
@article{fc2a7749-008f-4922-a919-8697467b5177,
abstract = {{Background: S100A7 is an antimicrobial peptide involved in several inflammatory diseases. The aim of the present study was to explore the expression and regulation of S100A7 in seasonal allergic rhinitis (SAR). Methods: Nasal lavage (NAL) fluid was obtained from healthy controls before and after lipopolysaccharide (LPS) provocation, from SAR patients before and after allergen challenge, and from SAR patients having completed allergen-specific immunotherapy (ASIT). Nasal biopsies, nasal epithelial cells and blood were acquired from healthy donors. The airway epithelial cell line FaDu was used for in vitro experiments. Real-time RT-PCR and immunohistochemistry were used to determine S100A7 expression in nasal tissue and cells. Release of S100A7 in NAL and culture supernatants was measured by ELISA. The function of recombinant S100A7 was explored in epithelial cells, neutrophils and peripheral blood mononuclear cells (PBMC). Results: Nasal administration of LPS induced S100A7 release in healthy non-allergic subjects. The level of S100A7 was lower in NAL from SAR patients than from healthy controls, and it was further reduced in the SAR group 6 h post allergen provocation. In contrast, ASIT patients displayed higher levels after completed treatment. S100A7 was expressed in the nasal epithelium and in glands, and it was secreted by cultured epithelial cells. Stimulation with IL-4 and histamine repressed the epithelial S100A7 release. Further, recombinant S100A7 induced activation of neutrophils and PBMC. Conclusions: The present study shows an epithelial expression and excretion of S100A7 in the nose after microbial stimulation. The levels are diminished in rhinitis patients and in the presence of an allergic cytokine milieu, suggesting that the antimicrobial defense is compromised in patients with SAR.}},
author = {{Kvarnhammar, Anne Mansson and Rydberg, Camilla and Jarnkrants, Malin and Eriksson, Mia and Uddman, Rolf and Benson, Mikael and Cardell, Lars-Olaf}},
issn = {{1465-9921}},
keywords = {{Th2 cytokines; lipopolysaccharide; seasonal allergic rhinitis; antimicrobial peptide; epithelium; allergen-specific immunotherapy}},
language = {{eng}},
publisher = {{BioMed Central (BMC)}},
series = {{Respiratory Research}},
title = {{Diminished levels of nasal S100A7 (psoriasin) in seasonal allergic rhinitis: an effect mediated by Th2 cytokines}},
url = {{https://lup.lub.lu.se/search/files/2085047/2544720.pdf}},
doi = {{10.1186/1465-9921-13-2}},
volume = {{13}},
year = {{2012}},
}