Document Detail


T cell inflammatory response, Foxp3 and TNFRS18-L regulation of peripheral blood mononuclear cells from patients with nasal polyps-asthma after staphylococcal superantigen stimulation.
MedLine Citation:
PMID:  20701615     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Staphylococcal superantigens may modulate airway inflammatory disease.
OBJECTIVE: We assessed the effect of Staphylococcus aureus enterotoxin B (SEB) on T cell activation in patients with nasal polyps and asthma, and its possible link to aspirin hypersensitivity.
METHODS: Leucocytes were isolated from five healthy subjects (controls), five asthmatics with nasal polyps without (NP-ATA) and five with aspirin-induced asthma (NP-AIA). Cells were incubated with increasing concentrations of SEB for 4 and 18 h. Release of T(H)1/T(H)2 cytokines was assessed by Cytometric Bead-Array. Foxp3 and TNFRS18-L expression were analysed by qPCR and flow cytometry.
RESULTS: After 4 and 18 h, SEB significantly increased IFN-gamma, IL-4, TNF-alpha, IL-5 and IL-2 concentrations in supernatants of both NP polyp groups compared with controls. Baseline Foxp3 was significantly decreased in both NP-asthma groups. Incubation with SEB for 4 h induced a limited up-regulation of Foxp3 in NP-AIA patients, which was switched off consecutively. Foxp3 was significantly up-regulated in the control group after 18 h, but not in the NP-asthmatic groups. In parallel, TNFRS18-L mRNA significantly increased after 18 h in the NP-asthma groups compared with control subjects. This molecule was highly expressed in CD11c(+)CD14(+) cells and its levels increased after 18 and 24 h culture in the NP-asthma patients.
CONCLUSION: SEB induces both T(H)1 and T(H)2 pro-inflammatory responses in patients with nasal polyps and asthma regardless of the presence of aspirin hypersensitivity. The nature of this response may be linked to a basal deficiency of Foxp3 observed in the NP-asthmatic patients and/or to the up-regulation of TNFRS18-L on monocytes/dendritic cell precursors.
Authors:
C A Pérez Novo; M Jedrzejczak-Czechowicz; A Lewandowska-Polak; C Claeys; G Holtappels; P Van Cauwenberge; M L Kowalski; C Bachert
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology     Volume:  40     ISSN:  1365-2222     ISO Abbreviation:  Clin. Exp. Allergy     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-12     Completed Date:  2011-01-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8906443     Medline TA:  Clin Exp Allergy     Country:  England    
Other Details:
Languages:  eng     Pagination:  1323-32     Citation Subset:  IM    
Affiliation:
Upper Airways Research Laboratory, Department of Otorhinolaryngology, Ghent University Hospital, De Pintelaan 185, Ghent, Belgium. Claudina.Pereznovo@UGent.be
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Asthma, Aspirin-Induced / immunology*
Cytokines / biosynthesis
Enterotoxins / immunology*
Female
Forkhead Transcription Factors / metabolism*
Humans
Leukocytes, Mononuclear
Lymphocyte Activation
Male
Middle Aged
Nasal Polyps / immunology*
Receptors, Nerve Growth Factor / metabolism*
Receptors, Tumor Necrosis Factor / metabolism*
Staphylococcus aureus / immunology*
Superantigens / immunology*
T-Lymphocytes / immunology*
Chemical
Reg. No./Substance:
0/Cytokines; 0/Enterotoxins; 0/FOXP3 protein, human; 0/Forkhead Transcription Factors; 0/Receptors, Nerve Growth Factor; 0/Receptors, Tumor Necrosis Factor; 0/Superantigens; 0/TNFRSF18 protein, human; 39424-53-8/enterotoxin B, staphylococcal

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