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V. Seamon, A. Azzarolo; Ovariectomy of Murine Model of Sjögren’s Syndrome Up–Regulates IL–10, IL–18 and IL–1ß Over Time . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1957.
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© ARVO (1962-2015); The Authors (2016-present)
Pro–inflammatory cytokines, IL–18 and IL–1ß, as well as IL–10, an anti–inflammatory cytokine, have been shown to be up–regulated in patients with Sjogren’s syndrome (SS). IL–10 and IL–18 levels have also been shown to correlate with the severity of SS. 90% of SS patients are women most of whom are post–menopausal, indicating a role for sex hormones in the pathology of the disease; however, not all post–menopausal women develop SS. Therefore we hypothesized that a decline in the serum levels of sex hormones in genetically predisposed individuals promotes an increase of IL–10, IL–18 and IL–1ß, which becomes more severe with time, in the lacrimal glands.
Six wks old C57BL/10SnJ, control, and NOD.B10–H2b, a mouse model of SS, were ovariectomized (OVX) or sham operated. After three days or one week, the lacrimal glands were removed, pooled, total RNA extracted and semi–quantitative RT–PCR analysis was performed for IL–10, IL–18 and IL–1ß.
NOD mice showed an increase in the expression of IL–10, 1L–18 and Il–1ß in the lacrimal gland after three days and one week OVX compared to sham operated animals. The increase of expression in these cytokines was significantly greater at one week compared to three days. No changes in the expression of IL–10, 1L–18 and Il–1ß were observed between the sham and OVX in C57BL/10SnJ mice in either experimental time.
These results support our hypothesis that reduction of the circulatory levels of sex hormones causes an overexpression of inflammatory mediators in genetically predisposed animals, and this response became more severe after one week OVX compared with three days. A lack of sex hormones seems to accelerate the development and persistence of SS pathology in genetically predisposed mice.
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