{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T14:42:15Z","timestamp":1780670535648,"version":"3.54.1"},"reference-count":76,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2005,2,1]],"date-time":"2005-02-01T00:00:00Z","timestamp":1107216000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Lyme disease is a chronic inflammatory disorder caused by the spirochetal bacterium, Borrelia burgdorferi. In vitro evidence suggests that binding of spirochetal lipoproteins to CD14, a pattern recognition receptor expressed on monocytes\/macrophages and polymorphonuclear cells, is a critical requirement for cellular activation and the subsequent release of proinflammatory cytokines that most likely contribute to symptomatology and clinical manifestations. To test the validity of this notion, we assessed the impact of CD14 deficiency on Lyme disease in C3H\/HeN mice. Contrary to an anticipated diminution in pathology, CD14\u2212\/\u2212 mice exhibited more severe and persistent inflammation than did CD14+\/+ mice. This disparity reflects altered gene regulation within immune cells that may engender the higher bacterial burden and serum cytokine levels observed in CD14\u2212\/\u2212 mice. Comparing their in vitro stimulatory activity, live spirochetes, but not lysed organisms, were a potent CD14-independent stimulus of cytokine production, triggering an exaggerated response by CD14\u2212\/\u2212 macrophages. Collectively, our in vivo and in vitro findings support the provocative notion that: 1) pattern recognition by CD14 is entirely dispensable for elaboration of an inflammatory response to B. burgdorferi, and 2) CD14-independent signaling pathways are inherently more destructive than CD14-dependent pathways. Continued study of CD14-independent signaling pathways may provide mechanistic insight into the inflammatory processes that underlie development of chronic inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.174.3.1539","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T22:29:10Z","timestamp":1398032950000},"page":"1539-1548","source":"Crossref","is-referenced-by-count":41,"title":["Signaling through CD14 Attenuates the Inflammatory Response to\n                    <i>Borrelia burgdorferi<\/i>\n                    , the Agent of Lyme Disease"],"prefix":"10.1093","volume":"174","author":[{"given":"Mohammed Rafii-El-Idrissi","family":"Benhnia","sequence":"first","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College , Albany, NY 12208"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danielle","family":"Wroblewski","sequence":"additional","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College , Albany, NY 12208"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muhammad Naveed","family":"Akhtar","sequence":"additional","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College , Albany, NY 12208"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raina A","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Pathology, Albany Medical College , Albany, NY 12208"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wendy","family":"Lavezzi","sequence":"additional","affiliation":[{"name":"Department of Pathology, Albany Medical College , Albany, NY 12208"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophie C","family":"Gangloff","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, University of Reims , Reims ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanna M","family":"Goyert","sequence":"additional","affiliation":[{"name":"Division of Molecular Medicine, North Shore-Long Island Jewish Research Institute, New York University School of Medicine , Manhasset, NY 11030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa J","family":"Caimano","sequence":"additional","affiliation":[{"name":"Center for Microbial Pathogenesis and Department of Pathology, University of Connecticut Health Center , Farmington, CT 06030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin D","family":"Radolf","sequence":"additional","affiliation":[{"name":"Center for Microbial Pathogenesis and Departments of Medicine and Genetics & Developmental Biology, University of Connecticut Health Center , Farmington, CT 06030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy J","family":"Sellati","sequence":"additional","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College , Albany, NY 12208"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2005,2,1]]},"reference":[{"key":"2026020212260066900_R1","first-page":"7","volume-title":"Arthritis Rheum.","year":"1977"},{"key":"2026020212260066900_R2","first-page":"22","volume-title":"J. 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