Open AccessCytokine release from the nasal mucosa and whole blood after experimental exposures to organic dusts
Author(s) -
Sigsgaard T,
BonefeldJørgensen E.C.,
Kjærgaard S.k,
Mamas S,
Pedersen O.f
Publication year - 2000
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.2000.16a25.x
Subject(s) - mucous membrane of nose , lipopolysaccharide , cytokine , immunology , nasal lavage , nasal cavity , tumor necrosis factor alpha , medicine , nasal administration , whole blood , pharmacology , chemistry , allergy , surgery
The aim of this study was to assess the cytokine response after nasal exposure to organic dusts. In a double blinded, crossover study five garbage workers with occupational airway symptoms and five healthy garbage workers were intranasally exposed to endotoxin (lipopolysaccharide LPS), β‐1,3‐ d ‐glucan (GLU), Aspergillus sp., compost or the saline dilute for 15 min. Nasal cavity volume and nasal lavage (NAL) were performed at baseline and 3, 6, 11 h postexposure. NAL was analysed with differential cell counts, cysteinyl‐leukotrienes, tumour necrosis factor α, interleukin (IL)‐1β, IL‐6 and IL‐8. A whole blood assay on cytokine‐release was performed with LPS and GLU. NAL cytokines neutrophils, lymphocytes and albumin increased significantly at 6 h after LPS exposure. GLU induced an increase in albumin and a slight increase in IL‐1β 6–11 h post exposure. In the WBA a significant increase in all cytokines after exposure to LPS as well as GLU was found. Significantly more cells were seen in NAL of the control group 6 h post LPS exposure. In conclusion lipopolysaccharide is the most potent inducer of inflammation in the nasal mucosa whereas compost and β‐1,3‐ d ‐glucan only induce minor changes. This reaction to lipopolysaccharide is attenuated in workers with occupational airway symptoms. In whole blood assay, however, β‐1,3‐ d ‐glucan also induces cytokine release, indicating a different protective effect of the nasal mucosa towards lipopolysaccharide and β‐1,3‐ d ‐glucan.