title: Osteoclasts in normal and adjuvant arthritis bone tissues express the mRNA for both type I and II interleukin-1 receptors.
abstract: Osteoclasts are known to play a crucial role in both physiologic and pathologic bone resorption. Moreover, it is generally agreed that IL-1 has powerful effects on osteoclastic bone resorption, although the precise cellular sites and mechanisms by which IL-1 mediates osteoclastic bone resorption remain unclear. In particular, it is still controversial whether osteoclasts can respond to IL-1 directly. The expression of mRNA for type I IL-1 receptor (IL-1RI) and type II IL-1 receptor (IL-1RII) in osteoclasts was investigated in normal and inflammatory bone tissues by in situ hybridization to determine whether osteoclasts are the target cells for IL-1 and to elucidate the mechanism by which IL-1 induces osteoclastic bone resorption. For this study, normal tibiae were obtained from newborn, young, and adult mice and rats, and inflammatory bone tissues with bone destruction were obtained from adjuvant arthritis rat models. The results showed that (a) both IL-1 receptors (IL-1RI and -II) mRNA were expressed by osteoclasts in all tissue sections of normal tibiae; (b) at the stage of the adjuvant arthritis studied, the IL-1RI mRNA was the most predominant message in osteoclasts present in the area with serious cartilage and bone destruction, whereas the expression level of IL-1RII mRNA in these osteoclasts was weak; and (c) both IL-1RI and -II mRNA were expressed by osteoblasts, as well as by osteocytes localized in the osteoid. In addition, these messages were also expressed by chondrocytes, but the signals were not detected in the chondrocytes in the zones of hypertrophy and provisional calcification. Our present study demonstrates for the first time that mouse and rat osteoclasts express IL-1RI and -II mRNA, which suggest that a primary effect of IL-1 on osteoclasts may be one of the mechanisms by which IL-1 mediates normal bone remodeling and pathologic bone resorption in chronic inflammatory diseases.
authors.affiliation: Department of Preventive Dentistry, Faculty of Dentistry, Kyushu University, Fukuoka, Japan.
authors.forename: L X
authors.initials: LX
authors.lastname: Xu
authors.forename: T
authors.initials: T
authors.lastname: Kukita
authors.forename: Y
authors.initials: Y
authors.lastname: Nakano
authors.forename: H
authors.initials: H
authors.lastname: Yu
authors.forename: T
authors.initials: T
authors.lastname: Hotokebuchi
authors.forename: T
authors.initials: T
authors.lastname: Kuratani
authors.forename: T
authors.initials: T
authors.lastname: Iijima
authors.forename: T
authors.initials: T
authors.lastname: Koga
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000378:metabolism*; D001862:Bone Resorption / Q000235:genetics; D001842:Bone and Bones / Q000737:chemistry*; D005260:Female; D015870:Gene Expression; D007378:Interleukins / Q000235:genetics; D051379:Mice; D010010:Osteoclasts / Q000737:chemistry*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew; D017207:Rats, Sprague-Dawley; D017472:Receptors, Interleukin-1 / Q000235:genetics*; D013977:Tibia / Q000737:chemistry
chemical_list: D007378:Interleukins; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1