Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1 (5-Year IF – 2.0)
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Index Copernicus  – 171.00; MNiSW – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2017, vol. 26, nr 3, May-June, p. 461–466

doi: 10.17219/acem/62218

Publication type: original article

Language: English

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IL-22 modulates inflammatory properties of human primary aortic smooth muscle cells

Paulina Gorzelak-Pabis1,A,B,C,D, Maciej Chałubiński1,A,B,C,D, Katarzyna Wojdan1,B,C, Emilia Łuczak1,B,C, Maciej Borowiec2,3,E, Marlena Broncel1,E,F

1 Laboratory of Tissue Immunopharmacology, Department of Internal Diseases and Clinical Pharmacology, Medical University of Lodz, Poland

2 Immunopathology and Genetics Laboratory, Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, Poland

3 Department of Clinical Genetics, Medical University of Lodz, Poland

Abstract

Background. IL-22 is expressed at barrier surfaces, which suggests its critical role in the maintenance of normal barrier homeostasis and tissue repair. IL-22 can both promote pathological inflammation and prevent the destruction of tissues. The functional outcomes of IL-22 on vascular smooth muscle cells, which are shown to regulate immune processes within the vascular wall and which are involved in certain pathologies, have not been analyzed.
Objectives. The effect of IL-22 on the expression of novel antiand pro-inflammatory and barrier disrupting cytokines, apoptosis and the expression of adhesive molecules in human primary aortic smooth muscle cells (AoSMC) was investigated.
Material and Methods. Human AoSMC were induced with IL-22 for 24 h in vitro. The influence of IL-22 on IL-35 subunits EBI3 and p35, IL-33, IFN-γ and VEGF mRNA expression in Ao-SMC were assessed using real-time PCR. Additionally, the surface expression of ICAM-1 and apoptosis of AoSMC were analyzed in the flow cytometer.
Results. IL-22 caused a 2- and 3-fold increase of mRNA expression of the EBI3 and p35 IL-35 subunits, and a 40% decrease of IL-33 mRNA expression in AoSMC. Additionally, IL-22 decreased ICAM-1 expression on the surface of AoSMC by 30%. However, IL-22 affected neither IFN-γ and VEGF mRNA expression in AoSMC nor their apoptosis and viability.
Conclusion. Our data suggest that IL-22, which is released by Th22 and NK cells, may be an agent affecting the inflammatory response of AoSMC, and thus it may regulate immune homeostasis of the vascular wall.

Key words

ICAM-1, IL-22, th22 cells, AoSMC

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