TITLE:
IL-1 Receptor Type II Production Is Upregulated by IL-4 and IL-13, and Downregulated by IFN-γ in Mouse Gingival Epithelial Cells
AUTHORS:
Y. Kamiya, Y. Ishihara, H. Kamei, Y. Ozawa, H. Mizutani, K. Kubo, H. Maeda, T. Noguchi
KEYWORDS:
IL-1RII, IL-4, IL-13, IFN-γ, STAT-6
JOURNAL NAME:
Modern Research in Inflammation,
Vol.3 No.2,
April
21,
2014
ABSTRACT: Background and Objective: Interleukin-1 (IL-1) binds to 2 distinct
and separate receptors, types I and II (IL-1RI and IL-1RII, respectively). The
binding of IL-1 to IL-1RI induces cellular signaling and biological effects,
whereas binding to IL-1RII does not induce cellular signaling and indirectly
inhibits IL-1 biological activities such as that of the decoy receptor.
Recently, Suzukiet al.reported that soluble IL-1RII (sIL-1RII) was detected in
gingival crevicular fluid from a periodontitis patient. However, it remains
unclear which cells produce sIL-1RII detected in periodontal tissues. We
examined the localization of IL-1RII producing cells in gingival tissues as
well as related production control mechanisms. Material and Methods: IL-1RII
mRNA expression in gingival epithelial cells (GE1) was performed by real-time
PCR analysis, while the amount of sIL-1RII production in supernatant from GE1
cells was examined by dot-blot analysis. Involvement of the phosphorylation of
STAT6 in the signaling pathway was determined by western blot analysis.
Statistical analysis was performed with Student’st-test. Results: Culturing
with IL-4 and IL-13 significantly increased IL-1RII mRNA to levels 10.5-and
8.89-fold, respectively, above that of the control (pγ (IFN-γ) significantly suppressed IL-1RII mRNA by 0.22-fold as
compared to the control (pγ, while western blotting determines the suppression of
IL-1RII production by IFN-γ. Without the addition of IL-4 or IL-13 with or without IFN-γ, P-Tyr-STAT6 was not detected. Conclusion: IL-1RII mRNA
expression and sIL-1RII production were increased by IL-4 and IL-13, and
decreased by IFN-γ. Finally, IL-4 signaling was regulated by IFN-γ through phosphorylation of
STAT6 and IL-13 signaling blockage by IFN-γ downstream of STAT6 translocation.