title: The effect of IL-1beta on the expression of inflammatory cytokines and their receptors in human chondrocytes.
abstract: Cytokines released at sites of inflammation and infection can alter the normal processes of cartilage turnover, resulting in pathologic destruction or formation. Interleukin (IL)-1beta plays a central role in the pathophysiology of cartilage damage and degradation in arthritis. In the present study, we examined the effect of IL-1beta on the expression of IL-1beta, IL-6, IL-8, IL-11, tumor necrosis factor-alpha (TNF-alpha), and their receptors in human chondrocytes. The cells were cultured either with or without 100 U/ml of IL-1beta for up to 28 days. The level of expression of the cytokines and their receptors was estimated by determining mRNA levels using real-time PCR or by determining protein levels using ELISA. The expression of IL-1beta, IL-8, and TNF-alpha markedly increased in the presence of IL-1beta after day 14 of culture. The expression of IL-6 and IL-11 increased greatly in the presence of IL-1beta on day 1 and after day 14 of culture. The expression of IL-1beta, IL-8, IL-11, and TNF-alpha receptors significantly decreased in the presence of IL-1beta after day 14 of culture, whereas the expression of IL-6 receptor significantly increased. The expression of these cytokines, except for IL-6, decreased with the addition of human IL-1 receptor antagonist. These results suggest that IL-1beta promotes the resolution system of cartilage matrix turnover through an increase in inflammatory cytokine production by chondrocytes and that it also may promote the autocrine action of IL-6 through an increase in IL-6 receptor expression in the cells.
authors.affiliation: Department of Crown and Bridge Prosthodontics, Nihon University School of Dentistry, 1-8-13 Kanda Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Aida
authors.forename: Masao
authors.initials: M
authors.lastname: Maeno
authors.forename: Naoto
authors.initials: N
authors.lastname: Suzuki
authors.forename: Aki
authors.initials: A
authors.lastname: Namba
authors.forename: Masafumi
authors.initials: M
authors.lastname: Motohashi
authors.forename: Mitsuhiko
authors.initials: M
authors.lastname: Matsumoto
authors.forename: Masaharu
authors.initials: M
authors.lastname: Makimura
authors.forename: Hideo
authors.initials: H
authors.lastname: Matsumura
mesh_terms: D019898:Autocrine Communication; D048430:Cell Shape; D002478:Cells, Cultured; D019902:Chondrocytes / Q000737:chemistry* / Q000166:cytology / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics*; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D007249:Inflammation; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000494:pharmacology*; D015850:Interleukin-6 / Q000235:genetics / Q000502:physiology; D018121:Receptors, Cytokine / Q000096:biosynthesis / Q000235:genetics*; D012795:Sialoglycoproteins / Q000494:pharmacology
chemical_list: D016207:Cytokines; C507763:IL1RN protein, human; C508600:IL6 protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D015850:Interleukin-6; D018121:Receptors, Cytokine; D012795:Sialoglycoproteins