Description
Presentation Blocks: 03-22-2018 - Thursday - 11:00 AM - 12:15 PM

Title: CXCL1-mediated Signaling Pathway in Response to P.g./LPS in THP-1

Authors:

Abdullah Bamashmous (Presenter)
Boston University

Serge Dibart, Boston University
Xiaoren Tang, Boston University
Erdjan Salih, Boston University

Abstract:

Objectives: CXCL1, a human chemokine, is well known to be involved in inflammatory diseases. However, the mechanism of CXCL1 in P.g/LPS-mediated signaling pathway is not clear yet. Our project is to find out CXCL1-dependent signaling pathway in human THP-1 cells in response to P.g/LPS

Methods: The CXCL1 cDNA was cloned into pcDNA3. Co-treatment of CXCL1 with inhibitor in THP-1 cells were performed and their media were measured by ELISA with the antibody against TNF-alpha/IL-1beta or the protein from the treated group was detected by Western blot with antibodies. detected Mutagenesis was used to make DNA site mutation.

Results: Our preliminary data showed that expression of CXCL1 significantly regulates LPS/P.g-induced TNF-alpha production via JAK or PI3K. The other kinase such NFkB, MEK, p38,MAPK, or Akt were not related with this regulation. We also found that the transient transfection of CXCL1 in THP-1 cells induced both TNF-alpha and IL-1beta. Furthermore, co-treatment of CXCL1 cDNA with LPS/P.g in THP-1 cells increased IL-1beta production much more than the control treated with CXCL1 alone. Finally, we described an assumed CXCL1-mediated signaling pathway in human THP-1 cells in response to LPS/P.g.

Conclusions: 1. Overexpression of CXCL1 cDNA alone in THP-1 cells induces TNF-a/IL-1 beta production.
2. Co-treatment of CXCL1 cDNA with LPS induces IL-1beta production in THP-1 cells
3. Inhibition of JAK in THP-1 cells decreases CXCL1-induced TNF-alpha/IL-1beta, meaning that JAK is a key kinase involved in CXCL1-mediated signaling pathway.

Schedule
poster

Poster Session

11:00 am–12:15 pm Mar 22 (US - Eastern)

CC, Hall B/C