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Lyme Disease symptoms vary from person to person. (lymes disease lyme's disease lime disease limes disease)
The data and information presented in this web site are presented in good faith and believed to be accurate regarding Lyme disease (commonly misspelled lymes disease lyme's disease lime disease limes disease) and other related diseases. Any and all liability for the content or any omissions including any inaccuracies, errors, or misstatements in such data or information is expressly disclaimed. The web site is compiled for the sole purpose of informing community members of resources and information pertaining to Lyme Borreliosis Disease and its coinfections. Lyme disease symptoms may vary from person to person.
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: J Immunol. 2005 Feb 1;174(3):1539-1548.
[Full text article at www.jimmunol.org]
Signaling through CD14 Attenuates the Inflammatory Response to Borrelia burgdorferi, the Agent of Lyme Disease.
Benhnia MR, Wroblewski D, Akhtar MN, Patel RA, Lavezzi W, Gangloff SC, Goyert SM, Caimano MJ, Radolf JD, Sellati TJ.
Center for Immunology and Microbial Disease and.
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(-/-) 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(-/-) 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(-/-) 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.
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