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- Interleukin-4 and interleukin-13 inhibit the expression of leukemia inhibitory factor and interleukin-11 in fibroblasts
- Umea Univ
- Universidade Estadual Paulista (UNESP)
- Univ Arkansas Med Sci
- Univ Gothenburg
- Swedish Research Council
- Swedish Dental Society
- Royal 80 Year Fund
- Swedish Rheumatism Association
- Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
- Cytokines produced by inflammatory or resident mesenchymal cells play important modulatory roles in the pathogenesis of inflammation induced bone loss. In the present study, the effects of IL-4 and IL-13 on the expression of three osteotropic cytokines in the IL-6 family expressed in human gingival fibroblasts were studied. IL-4R alpha and IL-13R alpha 1 mRNA were constitutively expressed in human gingival fibroblasts. The inflammatory cytokines IL-1 beta and TNF-alpha increased expression of IL-5, LIF, and IL-11 mRNA and protein in the gingival fibroblasts. Addition of IL-4 or IL-13 had no effect on IL-6 expression, but significantly inhibited LIF and IL-11 mRNA and protein stimulated by IL-1 beta and TNF-alpha. No involvement of NF-kappa B or STAT1 was observed in the inhibition. STAT6 was phosphorylated at Y641 by treatment with IL-4 and knockdown of STAT6 with siRNA decreased the inhibition of IL-11 and LIF expression by IL-4 in IL-1 beta and TNF-alpha stimulated cells. This study suggests that activation of STAT6 by IL-4 and IL-13, through type 2 IL-4 receptors, inhibits production of IL-11 and LIF stimulated by IL-1 beta and TNF-alpha in human gingival fibroblasts. A negative modulatory role of IL-4 and IL-13 in osteotropic cytokine production could be a mechanism playing an important inhibitory role in inflammation induced periodontitis. (C) 2011 Elsevier Ltd. All rights reserved.
- Molecular Immunology. Oxford: Pergamon-Elsevier B.V. Ltd, v. 49, n. 4, p. 601-610, 2012.
- Pergamon-Elsevier B.V. Ltd
- Gingival fibroblasts
- Bone resorption
- Acesso restrito
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