Rheumatology (Oxford, England) · 2012
Increased expression of interleukin-32 in the inflamed ileum of ankylosing spondylitis patients.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Ciccia Francesco, Rizzo Aroldo, Accardo-Palumbo Antonina, Giardina Annarita, Bombardieri Michele, Guggino Giuliana, Taverna Simona, Leo Giacomo De, Alessandro Riccardo, Triolo Giovanni
Аннотация
OBJECTIVE: To study the mRNA expression and protein tissue distribution of IL-32 in ileal biopsy specimens from patients with AS.
METHODS: Quantitative gene expression analysis, by real-time PCR, of IL-32, IL-1β, IL-10, TNF-α and IFN-γ was performed on ileal biopsies of 15 AS and 15 Crohn's disease (CD) patients and 10 healthy subjects (HSs). IL-32 tissue distribution was evaluated by immunohistochemistry. The effect of IL-32 on the production of IL-10 by intestinal epithelial cell lines was also evaluated.
RESULTS: In the ileal specimens of patients with AS and intestinal chronic inflammation, significant up-regulation of IL-32 at both the mRNA and protein levels was found as compared with non-inflamed AS patients and controls. IL-32 over-expression in AS was accompanied by a significant increase of IL-10 but not of cytokines involved in IL-32 induction. IL-32 stimulates intestinal epithelial cell lines in vitro to produce IL-10.
CONCLUSION: Our findings suggest IL-32 as an important cytokine probably involved in the innate immune response occurring in early phases of intestinal inflammation, where it seems to play a prevalent protective role.
METHODS: Quantitative gene expression analysis, by real-time PCR, of IL-32, IL-1β, IL-10, TNF-α and IFN-γ was performed on ileal biopsies of 15 AS and 15 Crohn's disease (CD) patients and 10 healthy subjects (HSs). IL-32 tissue distribution was evaluated by immunohistochemistry. The effect of IL-32 on the production of IL-10 by intestinal epithelial cell lines was also evaluated.
RESULTS: In the ileal specimens of patients with AS and intestinal chronic inflammation, significant up-regulation of IL-32 at both the mRNA and protein levels was found as compared with non-inflamed AS patients and controls. IL-32 over-expression in AS was accompanied by a significant increase of IL-10 but not of cytokines involved in IL-32 induction. IL-32 stimulates intestinal epithelial cell lines in vitro to produce IL-10.
CONCLUSION: Our findings suggest IL-32 as an important cytokine probably involved in the innate immune response occurring in early phases of intestinal inflammation, where it seems to play a prevalent protective role.