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CD14 Modulates PI3K/AKT/p38-MAPK Licensing of Negative Regulators of TLR Signaling to Restrain Chronic Inflammation
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- Albany Medical College, Center for Immunology and Microbial Disease
- Rensselaer Polytechnic Institute, Department of Biology
- Quinnipiac University, Department of Biomedical Sciences
- University of Connecticutt Health Center, Center for Microbial Pathogenesis
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- Document Type:
- Manuscript
- Date:
- Received 24 June 2008 18:09 UTC; Posted 25 June 2008
- Subjects:
- Immunology, Microbiology
- Abstract:
Current thinking emphasizes the primacy of CD14 in facilitating TLR recognition of microbes to initiate proinflammatory signaling events and the importance of p38-MAPK in augmenting such responses. Herein, this paradigm is challenged by demonstrating that recognition of Borrelia burgdorferi not only triggers an inflammatory response in the absence of CD14, but one that is uncontrolled as a consequence of impaired PI3K/AKT/p38-MAPK signaling and negative regulation of TLR2. CD14 deficiency results in hyperphosphorylation of AKT and reduced activation of p38. Such aberrant signaling leads to decreased negative regulation by SOCS1, SOCS3, and CIS thereby engendering a more severe and persistent inflammatory response to B. burgdorferi. Perturbation of this CD14/p38-MAPK-dependent mechanism of immune regulation may underlie development of infectious chronic inflammatory syndromes.
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- This document is licensed to the public under the Creative Commons Attribution 3.0 License
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Sahay, Bikash, Patsey, Rebeca, Whatley, Nicole, Nayak, Sasmita, Eggers, Christian, Radolf, Justin, and Sellati, Timothy. CD14 Modulates PI3K/AKT/p38-MAPK Licensing of Negative Regulators of TLR Signaling to Restrain Chronic Inflammation. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2008.2005.1> (2008)
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Bikash Sahay on 27 June 2008 14:24 UTC
It is a nice description of the differences attributed by the live bacteria and killed bacteria. It also showed a different role of p38 as an anti-inflammatory activity.