{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:17:44Z","timestamp":1789971464600,"version":"4.0.1"},"reference-count":85,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2013,5,25]],"date-time":"2013-05-25T00:00:00Z","timestamp":1369440000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The catabolic cytokine interleukin\u20101 (IL\u20101) and endotoxin lipopolysaccharide (LPS) are well\u2010known inflammatory mediators involved in degenerative disc disease, and inhibitors of IL\u20101 and LPS may potentially be used to slow or prevent disc degeneration in vivo. Here, we elucidate the striking anti\u2010catabolic and anti\u2010inflammatory effects of bovine lactoferricin (LfcinB) in the intervertebral disc (IVD) via antagonism of both IL\u20101 and LPS\u2010mediated catabolic activity using in vitro and ex vivo analyses. Specifically, we demonstrate the biological counteraction of LfcinB against IL\u20101 and LPS\u2010mediated proteoglycan (PG) depletion, matrix\u2010degrading enzyme production, and enzyme activity in long\u2010term (alginate beads) and short\u2010term (monolayer) culture models using bovine and human nucleus pulposus (NP) cells. LfcinB significantly attenuates the IL\u20101 and LPS\u2010mediated suppression of PG production and synthesis, and thus restores PG accumulation and pericellular matrix formation. Simultaneously, LfcinB antagonizes catabolic factor mediated induction of multiple cartilage\u2010degrading enzymes, including MMP\u20101, MMP\u20103, MMP\u201013, ADAMTS\u20104, and ADAMTS\u20105, in bovine NP cells at both mRNA and protein levels. LfcinB also suppresses the catabolic factor\u2010induced stimulation of oxidative and inflammatory factors such as iNOS, IL\u20106, and toll\u2010like receptor\u20102 (TLR\u20102) and TLR\u20104. Finally, the ability of LfcinB to antagonize IL\u20101 and LPS\u2010mediated suppression of PG is upheld in an en bloc intradiscal microinjection model followed by ex vivo organ culture using both mouse and rabbit IVD tissue, suggesting a potential therapeutic benefit of LfcinB on degenerative disc disease in the future. J. Cell. Physiol. 228: 1884\u20131896, 2013. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcp.24350","type":"journal-article","created":{"date-parts":[[2013,3,5]],"date-time":"2013-03-05T02:19:34Z","timestamp":1362449974000},"page":"1884-1896","source":"Crossref","is-referenced-by-count":65,"title":["Lactoferricin mediates anti\u2010inflammatory and anti\u2010catabolic effects via inhibition of IL\u20101 and LPS activity in the intervertebral disc"],"prefix":"10.1002","volume":"228","author":[{"given":"Jae\u2010Sung","family":"Kim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael B.","family":"Ellman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongyao","family":"Yan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard 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