An interleukin 1 like factor stimulates bone resorption in vitro

Abstract

Many activities are now ascribed to the monokine interleukin 1 including enhancement of immune responses, stimulation of thymocyte proliferation, activation of B cells, stimulation of proteinase and prostaglandin production by connective tissue cells, stimulation of the production of acute phase proteins, induction of fever and the induction of neutrophilia. These activities were thought to be due to various different factors, but are now considered probably due to very similar, if not identical, molecules. The term interleukin 1 (IL-1) was coined to describe the factor released by monocyte/macrophages which acts on T and B lymphocytes. Only after this definition had been accepted was it shown that target cells other than lymphocytes were affected by IL-1. Products of human blood monocytes (mononuclear cell factor, MCF) have been implicated in the pathogenesis of inflammatory diseases such as rheumatoid arthritis and periodontal disease. Bone resorption is often a feature of such diseases, and monocytes are frequently found at sites of localized bone resorption. Preliminary experiments with monocyte-conditioned medium indicated that MCF could stimulate bone resorption. We therefore undertook this study to verify these observations and to determine whether purified IL-1 could stimulate connective tissue breakdown in vitro.

Polymorphisms in the interleukin‐1 receptor antagonist and interleukin‐6 genes affect risk of osteolysis in patients with total hip arthroplasty

“…The proinflammatory cytokines IL-1␣ and IL-1␤ bind to IL-1 receptor type I (IL-1RI) and initiate cellular signaling. Both IL-1␣ and IL-1␤ induce increased osteoclast formation and activation, effects that are mediated through RANKL (9,10). IL-1R antagonist (IL-1Ra) also binds to IL-1RI and acts as a competitive antagonist to signal transduction (11).…”

Common variants in genes that mediate immunity and risk of multiple myeloma

“…IL-6 is considered the primary mediator contributing to the autocrine 51 and paracrine monoclonal expansion [52][53][54][55][56] and survival 57,58 of MM tumor cells both in the bone marrow microenvironment and in vitro. TNF-a is 1 factor known to induce IL-6 expression, 59 and thus, it may contribute to MM pathogenesis indirectly via the paracrine upregulation of IL-6 or directly by inhibiting bone resorbtion, 60,61 which subsequently facilitates the development of osteolytic bone disease observed in patients with advanced-staged disease. 62,63 Although haplotypes of VCAM1 and CARD15 were associated with increased risk of MM, these relationships did not achieve statistical significance.…”

Study of Serum Calcium, Microalbuminuria, Urinary Calcium/Creatinine Ratio in Postmenopausal Women

“…Intestinal calcium absorption decreases in postmenopausal women. (9) Calcium, well known as a bone resorption marker, is recommended as biochemical marker for osteoporosis screening.…”