Serum cytokine and chemokine levels in patients with eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, or eosinophilic asthma.
Journal
Clinical and experimental rheumatology
ISSN: 0392-856X
Titre abrégé: Clin Exp Rheumatol
Pays: Italy
ID NLM: 8308521
Informations de publication
Date de publication:
Historique:
received:
17
03
2018
accepted:
22
05
2018
pubmed:
18
1
2019
medline:
15
6
2019
entrez:
18
1
2019
Statut:
ppublish
Résumé
The pathogenesis of eosinophilic granulomatosis with polyangiitis (EGPA) remains poorly understood, and may overlap with eosinophilic asthma and primary hypereosinophilic syndrome (HES). The aim of this study was to analyse a panel of serum cytokines and chemokines as markers of disease activity in patients with these conditions. The levels of 54 cytokines and chemokines were measured in the sera of 40 patients with active EGPA, 10 of these patients during inactive disease, 6 patients with HES, 8 with asthma, and 10 healthy controls. Serum cytokine/chemokines measured included interleukin (IL)-1α, 1β, 3, 4, 5, 6, 8, 13, 15, 17A, 17E(25), 18, 23 and 33, soluble IL-2 receptor alpha, eotaxin-1 (CCL11), -2 (CCL24) and -3 (CCL26), macrophage-derived chemokine (MDC/CCL22), macrophage inflammatory protein (MIP)-1a and -1b, and tumour necrosis factor (TNF)-α. Results were compared between disease and control groups using regression analysis, with Bonferroni correction for multiple comparisons (significant p value ≤0.00093). Significant differences were observed only in serum levels of MDC, IL-8, MIP-1a and -1b, TNF-α, each of which were lower in patients with active EGPA than in healthy controls (p<0.0001). Differences between patients with active disease and other disease groups did not reach significance. Paired comparisons between sera from patients with active or inactive EGPA showed no significant difference for any of the studied cytokines or chemokines. No clear difference in the serum levels of measured cytokines and chemokines helped distinguish between active EGPA or inactive EGPA, or other disease or control groups.
Identifiants
pubmed: 30652675
pii: 12801
pmc: PMC9878582
mid: NIHMS1863819
Substances chimiques
Biomarkers
0
Chemokines
0
Cytokines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
40-44Subventions
Organisme : NIAMS NIH HHS
ID : U54 AR057319
Pays : United States
Organisme : NCRR NIH HHS
ID : U54 RR019497
Pays : United States
Références
Immunology. 1994 Aug;82(4):591-5
pubmed: 7835922
Arthritis Rheum. 1990 Aug;33(8):1094-100
pubmed: 2202307
J Leukoc Biol. 2000 Sep;68(3):400-4
pubmed: 10985257
Ann Rheum Dis. 2013 Aug;72(8):1342-50
pubmed: 22975753
Eur J Intern Med. 2015 Sep;26(7):545-53
pubmed: 25971154
Clin Chem Lab Med. 2013 Jul;51(7):1385-93
pubmed: 23314551
Int J Biochem Cell Biol. 2004 Oct;36(10):1882-6
pubmed: 15203102
J Allergy Clin Immunol. 2012 Sep;130(3):607-612.e9
pubmed: 22460074
Ann N Y Acad Sci. 2005 Jun;1051:121-31
pubmed: 16126951
Allergy. 2012 Sep;67(9):1149-56
pubmed: 22775568
Arthritis Rheum. 2013 Jan;65(1):1-11
pubmed: 23045170
Arthritis Rheum. 2010 Nov;62(11):3496-503
pubmed: 20669282
Rheumatology (Oxford). 2015 Aug;54(8):1351-9
pubmed: 25406357
Rheumatology (Oxford). 2008 Jun;47(6):804-8
pubmed: 18397958
Rheumatology (Oxford). 2011 Oct;50(10):1823-7
pubmed: 21266446
Scand J Rheumatol. 2012 Oct;41(5):403-5
pubmed: 23043346
Arthritis Rheum. 2013 Jan;65(1):270-81
pubmed: 23044708
Medicine (Baltimore). 1975 Jan;54(1):1-27
pubmed: 1090795
Stat Med. 1990 Jul;9(7):811-8
pubmed: 2218183
PLoS One. 2015 Mar 26;10(3):e0121737
pubmed: 25812008