RII Track-4: Characterization of LPS-induced Hsc70 ligands as a means of defining the role of C-linked glycosylation in innate immunity.

Information

  • NSF Award
  • 1738707
Owner
  • Award Id
    1738707
  • Award Effective Date
    9/1/2017 - 7 years ago
  • Award Expiration Date
    8/31/2019 - 5 years ago
  • Award Amount
    $ 160,614.00
  • Award Instrument
    Standard Grant

RII Track-4: Characterization of LPS-induced Hsc70 ligands as a means of defining the role of C-linked glycosylation in innate immunity.

Non-technical Description<br/>The immune system's response to infection and autoimmune diseases includes inflammation that is controlled by specific chemicals, and the production and function of many of which is not clearly understood. This project supports the PI for a six-month period in the Complex Carbohydrate Research Center (CCRC) at the University of Georgia. The CCRC possesses unparalleled research expertise and analytical instrumentation focused on the biochemical study of carbohydrate molecules, including those involved in inflammation. This fellowship allows the PI access to the expertise and the advanced instrumentation capability of CCRC, and he will bring that expertise back to Marshall University. Characterization of these molecules in the context of inflammation will provide important information about the causes and control of inflammation, including inflammation involved in autoimmune disease. <br/><br/>Technical Description<br/>This fellowship will aid in bolstering the research capacity in West Virginia by supporting the PI's efforts to use the resources at the CCRC to evaluate protein regulators of the innate immune response. Providing access to the facilities and expertise at the CCRC will enable the PI to establish a vibrant research program studying the role of glycosylation in inflammation in West Virginia. It has been shown that C-glycosylated peptides enhance the production of the proinflammatory cytokine TNF&#945;, secreted from lipopolysaccharide (LPS)-stimulated macrophage-like cells. This indicates that a currently unknown regulatory mechanism involving C-linked glycosylation is crucial for activation of the LPS/TLR4 pathway. As TNF&#945; is the central cytokine produced in the inflammatory response, defining how C-linked glycosylation regulates this cytokine response is critical in properly addressing its dysregulation. Dysregulation of TNF&#945; is inherent to inflammatory diseases such as Crohn?s disease, sepsis, rheumatoid arthritis, and metabolic syndrome.

  • Program Officer
    Raffaella Montelli
  • Min Amd Letter Date
    9/12/2017 - 7 years ago
  • Max Amd Letter Date
    9/12/2017 - 7 years ago
  • ARRA Amount

Institutions

  • Name
    Marshall University Research Corporation
  • City
    Huntington
  • State
    WV
  • Country
    United States
  • Address
    One John Marshall Dr.
  • Postal Code
    257550002
  • Phone Number
    3046964837

Investigators

  • First Name
    John
  • Last Name
    Rakus
  • Email Address
    rakus@marshall.edu
  • Start Date
    9/12/2017 12:00:00 AM

Program Element

  • Text
    RESEARCH INFRASTRUCTURE IMPROV
  • Code
    7217

Program Reference

  • Text
    EXP PROG TO STIM COMP RES
  • Code
    9150