Cytokine profile characterization of naïve patients with psoriasis and psoriatic arthritis: implications for a pathogenic disease continuum.
biomarkers
mechanistic biomarkers
psoriasis
psoriatic arthritis
psoriatic disease
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2023
2023
Historique:
received:
26
05
2023
accepted:
26
06
2023
medline:
1
8
2023
pubmed:
31
7
2023
entrez:
31
7
2023
Statut:
epublish
Résumé
The idea of psoriatic disease continuum has been progressively prompted based on the advances of the knowledge about the pathogenic steps underpinning the occurrence of psoriasis (PSO) and psoriatic arthritis (PSA). To evaluate biomolecules (inflammatory cytokines, inflammatory chemokines, cell adhesion and cellular mediators) in naïve patients with PSO, PSA with PSO, and PSA sine PSO. To stratify the results considering the presence of psoriatic nail involvement, extensive skin disease and obesity evaluating all involved patients. By multiplex technology, 20 serum biomolecules were assessed with the inclusion of pro-inflammatory cytokines (GM-CSF, IFN-γ, IL-1α, IL-1β, IL-6, IL-8, IL-12p70, IL-17A, IL-23, TNF), anti-inflammatory cytokines (IFN-α, IL-4, IL-10, IL-13), inflammatory chemokines (IP-10, MCP-1, MIP-1α, MIP-1β), cell adhesion and cellular mediators (ICAM-1, E-selectin, P-selectin). The assessment of possible statistical differences between the means of the three groups was performed by One-Way ANOVA. In addition, by non-parametric T-tests, we stratified the results according to selected clinical characteristics (psoriatic nail involvement, PASI ≥ 10, BMI ≥ 30). In 80 assessed naïve patients, patients with PSO showed significant increases of E-selectin (p=0.021) and IL-8 (0.041) than other groups. In patients with PSA with PSO, significant higher levels of ICAM-1 were observed (p=0.009) than other groups. We did not observe further differences comparing pro-inflammatory and anti-inflammatory cytokines, inflammatory chemokines, and cell adhesion and cellular mediators in patients with PSO, PSA with PSO, and PSA sine PSO. Patients with psoriatic onychopathy showed significant increased levels of ICAM-1 (p=0.010) and IP-10 (0.030) than others. In patients with PASI ≥ 10, significantly enhanced values of IL-8 (p=0.004), TNF (p=0.013), E-selectin (p=0.004), MIP-1α (p=0.003), and MIP-1β (p=0.039). In patients with BMI ≥ 30, significantly higher levels of E-selectin were pointed out (p=0.035) than others. Our findings may suggest that a similar cytokine profile may characterize naïve patients with PSO, PSA with PSO, and PSA sine PSO, reinforcing the concept of psoriatic disease continuum. However, some differences may be also shown, underlying possible pathogenic differences and leading to the clinical heterogeneity of these patients.
Sections du résumé
Background
The idea of psoriatic disease continuum has been progressively prompted based on the advances of the knowledge about the pathogenic steps underpinning the occurrence of psoriasis (PSO) and psoriatic arthritis (PSA). To evaluate biomolecules (inflammatory cytokines, inflammatory chemokines, cell adhesion and cellular mediators) in naïve patients with PSO, PSA with PSO, and PSA sine PSO. To stratify the results considering the presence of psoriatic nail involvement, extensive skin disease and obesity evaluating all involved patients.
Methods
By multiplex technology, 20 serum biomolecules were assessed with the inclusion of pro-inflammatory cytokines (GM-CSF, IFN-γ, IL-1α, IL-1β, IL-6, IL-8, IL-12p70, IL-17A, IL-23, TNF), anti-inflammatory cytokines (IFN-α, IL-4, IL-10, IL-13), inflammatory chemokines (IP-10, MCP-1, MIP-1α, MIP-1β), cell adhesion and cellular mediators (ICAM-1, E-selectin, P-selectin). The assessment of possible statistical differences between the means of the three groups was performed by One-Way ANOVA. In addition, by non-parametric T-tests, we stratified the results according to selected clinical characteristics (psoriatic nail involvement, PASI ≥ 10, BMI ≥ 30).
Results
In 80 assessed naïve patients, patients with PSO showed significant increases of E-selectin (p=0.021) and IL-8 (0.041) than other groups. In patients with PSA with PSO, significant higher levels of ICAM-1 were observed (p=0.009) than other groups. We did not observe further differences comparing pro-inflammatory and anti-inflammatory cytokines, inflammatory chemokines, and cell adhesion and cellular mediators in patients with PSO, PSA with PSO, and PSA sine PSO. Patients with psoriatic onychopathy showed significant increased levels of ICAM-1 (p=0.010) and IP-10 (0.030) than others. In patients with PASI ≥ 10, significantly enhanced values of IL-8 (p=0.004), TNF (p=0.013), E-selectin (p=0.004), MIP-1α (p=0.003), and MIP-1β (p=0.039). In patients with BMI ≥ 30, significantly higher levels of E-selectin were pointed out (p=0.035) than others.
Conclusion
Our findings may suggest that a similar cytokine profile may characterize naïve patients with PSO, PSA with PSO, and PSA sine PSO, reinforcing the concept of psoriatic disease continuum. However, some differences may be also shown, underlying possible pathogenic differences and leading to the clinical heterogeneity of these patients.
Identifiants
pubmed: 37520537
doi: 10.3389/fimmu.2023.1229516
pmc: PMC10373502
doi:
Substances chimiques
E-Selectin
0
Intercellular Adhesion Molecule-1
126547-89-5
Chemokine CCL3
0
Chemokine CCL4
0
Chemokine CXCL10
0
Interleukin-8
0
Cytokines
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1229516Informations de copyright
Copyright © 2023 Ruscitti, Esposito, Di Cola, Pellegrini, De Berardinis, Mastrangelo, Gianneramo, Barile, Fargnoli and Cipriani.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
J Rheumatol. 2019 Nov;46(11):1428-1430
pubmed: 31676545
Arthritis Rheumatol. 2016 Dec;68(12):2911-2916
pubmed: 27389865
Arthritis Rheum. 2006 Aug;54(8):2665-73
pubmed: 16871531
Arthritis Rheum. 2008 Jun;58(6):1796-802
pubmed: 18512820
Int J Mol Sci. 2022 Nov 01;23(21):
pubmed: 36362116
Ann Rheum Dis. 2023 Jun 9;:
pubmed: 37295926
Autoimmun Rev. 2022 Dec;21(12):103207
pubmed: 36191778
Nat Rev Rheumatol. 2019 Mar;15(3):153-166
pubmed: 30742092
Rheumatol Ther. 2021 Dec;8(4):1725-1739
pubmed: 34564835
Br J Dermatol. 2020 Nov;183(5):920-927
pubmed: 32037514
Rheumatol Int. 2023 Aug;43(8):1525-1529
pubmed: 37017711
Afr Health Sci. 2022 Jun;22(2):286-294
pubmed: 36407366
Asian Pac J Trop Med. 2014 Jul;7(7):582-4
pubmed: 25063291
J Endocrinol Invest. 2023 Apr 18;:
pubmed: 37071373
Autoimmun Rev. 2014 Apr-May;13(4-5):490-5
pubmed: 24434359
Clin Exp Dermatol. 1999 Jan;24(1):33-6
pubmed: 10233646
Br J Dermatol. 2022 Oct;187(4):481-493
pubmed: 35482474
Cell Mol Immunol. 2023 Mar;20(3):217-251
pubmed: 36725964
Dermatologica. 1978;157(4):238-44
pubmed: 357213
Br J Dermatol. 2013 Aug;169(2):266-82
pubmed: 23550658
Nat Rev Rheumatol. 2013 May;9(5):267-76
pubmed: 23419428
Nat Rev Rheumatol. 2022 Sep;18(9):513-526
pubmed: 35927578
Nat Rev Rheumatol. 2021 Apr;17(4):238-243
pubmed: 33589818
Biomed Pharmacother. 2023 Mar;159:114294
pubmed: 36706632
Best Pract Res Clin Rheumatol. 2022 Dec;36(4):101809
pubmed: 36567224
ISRN Dermatol. 2013 May 30;2013:630620
pubmed: 23819059
Int J Mol Sci. 2023 Mar 28;24(7):
pubmed: 37047357
Ann Rheum Dis. 2022 Jan;81(1):68-73
pubmed: 34144965
Clin Immunol. 2020 Feb;211:108318
pubmed: 31783160
Radiol Med. 2022 Dec;127(12):1400-1406
pubmed: 36260243
Int J Mol Sci. 2023 Mar 03;24(5):
pubmed: 36902329
Br J Dermatol. 1996 Jan;134(1):17-21
pubmed: 8745880
Ther Adv Musculoskelet Dis. 2019 Nov 06;11:1759720X19886505
pubmed: 31723358
J Am Acad Dermatol. 2003 Aug;49(2):206-12
pubmed: 12894066
Nat Rev Rheumatol. 2022 Jun;18(6):311-325
pubmed: 35513599