IL-33 Enhanced the Proliferation and Constitutive Production of IL-13 and IL-5 by Fibrocytes

• Published in: BioMed research international 2014-01, Vol.2014 (2014), p.1-10
• Main Authors: Hayashi, Hisako, Kawakita, Akiko, Okazaki, Shintaro, Murai, Hiroki, Yasutomi, Motoko, Ohshima, Yusei
• Format: Article
• Language: English
• Subjects: Acetates - pharmacology; Actins - metabolism; Allergies; Angiogenesis; Cell culture; Cell growth; Cell Proliferation - drug effects; Cell Proliferation - physiology; Cells, Cultured; Cytokines; Dexamethasone - pharmacology; Humans; Immune system; Interleukin-1 Receptor-Like 1 Protein; Interleukins - analysis; Interleukins - metabolism; Interleukins - pharmacology; Leukocytes, Mononuclear - cytology; Leukocytes, Mononuclear - metabolism; Proteins; Quinolines - pharmacology; Receptors, Cell Surface - metabolism; Smooth muscle; Studies
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2014/738625

Interleukin-33 appears to play important roles in the induction of allergic airway inflammation. However, whether IL-33 is involved in airway remodeling remains unclear. Because fibrocytes contribute to tissue remodeling in the setting of chronic inflammation, we examined the effects of IL-33 on fibrocyte functions. Fibrocytes were generated in vitro from peripheral blood mononuclear cells by culturing in the presence of platelet derived growth factors and the cells were stimulated with IL-33. IL-33 enhanced cell proliferation, α-SMA expression, and pro-MMP-9 activity by the fibrocytes without increasing endogenous transforming growth factor-β1 production. Fibrocytes constitutively expressed IL-13 and IL-5, and their production was augmented by stimulation with IL-33. Dexamethasone inhibited the functions of fibrocytes, but IL-33 made fibrocytes slightly refractory to the inhibitory effect of dexamethasone in terms of IL-13 production. Montelukast suppressed IL-13 production by nonstimulated fibrocytes but not those stimulated by IL-33. These findings suggest that IL-33 is involved in the airway remodeling process through its modulation of fibrocyte function independent of antigen stimulation. IL-33 might partially reduce the therapeutic effects of glucocorticoid and cysteinyl leukotriene receptor antagonist on fibrocyte-mediated Th2 responses.