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FRI0023 Effects of IL-33/ST2 Axis on Cytokine Gene Expression at The Site of Acute Inflammation
  1. M. Stankovic1,
  2. K. Janjetovic2,
  3. N. Puskas3,
  4. M. Milenkovic2,
  5. I. Zaletel3,
  6. S.R. De Luka1,
  7. A.M. Trbovich1,
  8. V. Trajkovic2
  1. 1Department of Pathophysiology, School of Medicine University of Belgrade
  2. 2Institute of Microbiology and Immunology, School of Medicine University of Belgrade
  3. 3Institute of Histology and Embryology “Aleksandar Đ. Kostić”, School of Medicine University of Belgrade, Belgrade, Serbia

Abstract

Background Acute inflammation is an early response to a cell injury. Interleukin (IL)-33 is a new member of IL-1 cytokine family. It was discovered that IL-33 and its receptor ST2 have a role not only in Th2 mediated diseases, as firstly reported, but also in other diseases, such as rheumatoid arthritis, autoimmune uveitis, and squamous cell carcinoma. Effects of IL-33/ST2 axis in acute inflammation are still not completely understood.

Objectives The aim of this study was to examine effects of IL-33/ST2 axis on cytokine gene expression at the site of acute inflammation.

Methods Male mice were divided in groups: wild-type control group (WT-C), wild-type inflammatory group (WT-I), ST2 knockout control group (KO-C), and ST2 knockout inflammatory group (KO-I). Acute inflammation was induced in WT-I and KO-I by intramuscular injection of turpentine oil, whereas animals in WT-C and KO-C were injected with saline. Mice were euthanized after 12 hours, and the treated tissue was collected for histopathological analysis, and gene expression determination (qRT-PCR) of IL-33, ST2 receptor, tumor necrosis factor alpha (TNF-alpha), IL-12p35, IL-23p19, and transforming growth factor-beta (TGF-beta). All experimental procedures were approved by the University of Belgrade School of Medicine Ethics Committee.

Results Acute inflammation was histopathologicaly confirmed in WT-I and KO-I. IL-33 in the treated tissue was significantly higher in inflammatory groups, WT-I and KO-I, when compared to WT-C and KO-C, respectively. However, IL-33 was significantly higher in KO-I than in WT-I. ST2 significantly increased in inflamed tissue of wild-type mice, in comparison to WT-C. TNF-alpha, IL-12p35, and IL-23p19 in the treated tissue significantly increased in WT-I and KO-I, when compared to their corresponding control groups WT-C and KO-C. TGF-beta in the treated tissue was significantly higher in KO-I than in WT-I, whereas it did not significantly differ between WT-C and KO-C.

Conclusions Results of this study indicated that IL-33/ST2-axis affected gene expression of cytokines at the site of acute inflammation, i.e. gene expression of IL-33, and anti-inflammatory cytokine TGF-beta. ST2 gene expression increased in acutely inflamed tissue, indicating importance of IL-33/ST2 axis in acute inflammation.

  1. Verri et al. Ann Rheum Dis. 2010; 69(9):1697–1703; Barbour et al. Eur J Immunol. 2014; 44(11):3320–3329;

  2. Ishikawa et al. Auris Nasus Larynx. 2014; 41(6):552–557.

  3. Abbas et al. Cytokines. In Cellular and Molecular Immunology. 2010; 267–302.

Acknowledgement This research was funded by Ministry of Education, Science and Technological Development (RS, grant III 41013).

Disclosure of Interest None declared

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