{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T15:42:55Z","timestamp":1791474175545,"version":"4.3.4"},"reference-count":40,"publisher":"Springer Science and Business Media LLC","issue":"3","license":[{"start":{"date-parts":[[2012,5,21]],"date-time":"2012-05-21T00:00:00Z","timestamp":1337558400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"},{"start":{"date-parts":[[2012,5,21]],"date-time":"2012-05-21T00:00:00Z","timestamp":1337558400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Arthritis Res Ther"],"abstract":"<jats:title>Abstract\n<\/jats:title><jats:sec>\n                        <jats:title>Introduction\n<\/jats:title>\n                        <jats:p>The present study assessed the potential functions of interleukin (IL)-32\u03b1 on inflammatory arthritis and endotoxin shock models using IL-32\u03b1 transgenic (Tg) mice. The potential signaling pathway for the IL-32-tumor necrosis factor (TNF)\u03b1 axis was analyzed <jats:italic>in vitro<\/jats:italic>.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods\n<\/jats:title>\n                        <jats:p>IL-32\u03b1 Tg mice were generated under control of a ubiquitous promoter. Two disease models were used to examine <jats:italic>in vivo<\/jats:italic> effects of overexpressed IL-32\u03b1: Toll-like receptor (TLR) ligand-induced arthritis developed using a single injection of lipopolysaccharide (LPS) or zymosan into the knee joints; and endotoxin shock induced with intraperitoneal injection of LPS and D-galactosamine. TNF\u03b1 antagonist etanercept was administered simultaneously with LPS in some mice. Using RAW264.7 cells, <jats:italic>in vitro<\/jats:italic> effects of exogenous IL-32\u03b1 on TNF\u03b1, IL-6 or macrophage inflammatory protein 2 (MIP-2) production were assessed with or without inhibitors for nuclear factor kappa B (NF\u03baB) or mitogen-activated protein kinase (MAPK).<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results\n<\/jats:title>\n                        <jats:p>Single injection of LPS, but not zymosan, resulted in development of severe synovitis with substantial articular cartilage degradation in knees of the Tg mice. The expression of TNF\u03b1 mRNA in inflamed synovia was highly upregulated in the LPS-injected Tg mice. Moreover, the Tg mice were more susceptive to endotoxin-induced lethality than the wild-type control mice 48 hours after LPS challenge; but blockade of TNF\u03b1 by etanercept protected from endotoxin lethality. In cultured bone marrow cells derived from the Tg mice, overexpressed IL-32\u03b1 accelerated production of TNF\u03b1 upon stimulation with LPS. Of note, exogenously added IL-32\u03b1 alone stimulated RAW264.7 cells to express TNF\u03b1, IL-6, and MIP-2 mRNAs. Particularly, IL-32\u03b1 -induced TNF\u03b1, but not IL-6 or MIP-2, was inhibited by dehydroxymethylepoxyquinomicin (DHMEQ) and U0126, which are specific inhibitors of nuclear factor kappa B (NF\u03baB) and extracellular signal regulated kinase1\/2 (ERK1\/2), respectively.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions\n<\/jats:title>\n                        <jats:p>These results show that IL-32\u03b1 contributed to the development of inflammatory arthritis and endotoxin lethality. Stimulation of TLR signaling with LPS appeared indispensable for activating the IL-32\u03b1-TNF\u03b1 axis <jats:italic>in vivo<\/jats:italic>. However, IL-32\u03b1 alone induced TNF\u03b1 production in RAW264.7 cells through phosphorylation of inhibitor kappa B (I\u03baB) and ERK1\/2 MAPK. Further studies on the potential involvement of IL-32\u03b1-TNF\u03b1 axis will be beneficial in better understanding the pathology of autoimmune-related arthritis and infectious immunity.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/ar3850","type":"journal-article","created":{"date-parts":[[2012,5,21]],"date-time":"2012-05-21T12:14:45Z","timestamp":1337602485000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Enhanced susceptibility to lipopolysaccharide-induced arthritis and endotoxin shock in interleukin-32 alpha transgenic mice through induction of tumor necrosis factor alpha"],"prefix":"10.1186","volume":"14","author":[{"given":"Masanori","family":"Nakayama","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuo","family":"Niki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiki","family":"Kawasaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Takeda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keisuke","family":"Horiuchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aya","family":"Sasaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasunori","family":"Okada","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuo","family":"Umezawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyasu","family":"Ikegami","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiaki","family":"Toyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeshi","family":"Miyamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2012,5,21]]},"reference":[{"key":"3614_CR1","doi-asserted-by":"crossref","first-page":"597","DOI":"10.4049\/jimmunol.148.2.597","volume":"15","author":"CA Dahl","year":"1992","unstructured":"Dahl CA, Schall RP, He HL, Cairns JS: Identification of a novel gene expressed in activated natural killer cells and T cells. 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