Project Details
Abstract
The objective of this research is to investigate the cause of lung diseases by secreted
proteins from Mycobacterium tuberculosis. Previously, we have successfully cloned and
expressed the clone of ESAT-6/CFP-10 complex (CFES), combining cfp-10 with esat-6, and
utilized a cDNA array technology to analyse altered gene expressions of host cells causing by
secreting ESAT-6/CFP-10 in the infection process of Mycobacterium tuberculosis. By
utilizing bioinformatics tools, it have predicted the important biological hotpots and shown
the interaction of these genes. We found out the influence of CFES on the gene expression of
human lung cells involved cell proliferation, cell motility, cell survival and cell apoptosis.
And according to our preliminary results, it had verified CFES will cause chromosome
condensation and induce apoptosis. This proposal hypothesize that CFES induce an
apoptosis-related signal transduction enhanced the pathogenesis of M. tuberculosis. To prove
this hypothesis, we will investigate the influence of CFES on the signal transduction predicted
by cDNA microarray. The strategy combines the use of quantitative PCR, western blot and
immunoprecipitation methods to identify the gene expression, protein expression and their
involved signal transduction pathways. Once the signaling pathways have been identified, we
will block these pathways by using certain kinase inhibitors or siRNA knockdown for the key
proteins to observe if these interventions protect cells from CFES-induced apoptosis.
Furthermore, we will also observe the relationship between immunogenecity and
pathogenesis by treating WI-38 cells and THP1 cells with CFES. The results of this project
will help us understand the mechanism by which M. tuberculosis causes the pathogenesis.
Project IDs
Project ID:PC9801-2492
External Project ID:NSC97-2320-B182-014-MY3
External Project ID:NSC97-2320-B182-014-MY3
Status | Finished |
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Effective start/end date | 01/08/09 → 31/07/10 |
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