Open AccessInterleukin‐1 induces interleukin‐1α and interleukin‐1β gene expression in synovial fibroblasts and peripheral blood monocytes
Author(s) -
Dalton Barbara J.,
Connor Janice R.,
Johnson William J.
Publication year - 1989
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/anr.1780320309
Subject(s) - northern blot , interleukin , tumor necrosis factor alpha , synovial membrane , inflammation , collagenase , interleukin 4 , gene expression , fibroblast , immune system , cytokine , immunology , biology , microbiology and biotechnology , cell culture , gene , biochemistry , genetics , enzyme
Cellular interactions involved in the chronic inflammatory response, characteristic of those found in the joints of rheumatoid arthritis patients, were investigated by examining the effect of interleukin‐1 (IL‐1), tumor necrosis factor α, and γ‐interferon on the regulation of IL‐1 gene expression and production by synovial fibroblasts. Biologically active IL‐1 was detected in lysates of IL‐1–treated rat and human fibroblasts that had been isolated from synovial tissue by collagenase digestion. Northern blot analysis of RNA isolated from these cells revealed the expression of IL‐1α and IL‐1β transcripts. Neither the IL‐1 transcripts nor the biologic activity of IL‐1 was found in untreated synovial fibroblasts. The messenger RNA induction in synovial cells was followed by a time‐ and dose‐dependent expression of intracellular IL‐1 activity. Human monocytes and human skin fibroblasts also responded to IL‐1 treatment by producing IL‐1–specific transcripts. These observations suggest that IL‐1 plays a key role in stimulating immune and inflammatory responses and in sustaining those responses through continued production at sites of inflammation.