Recognition of Host Immune Activation by Pseudomonas aeruginosa

Speaker：黃思偉                                                           Time：5/17/2006 15:10~16:00

Commentator：何漣漪 老師                                 Place：Room 601

Abstract：

Cell-to-cell communication in bacteria termed quorum-sensing regulates many population activities such as virulence factor production, biofilm development and antibiotics resistance. Generally knowing that the opportunistic pathogens can monitor alteration of the host immune status and upregulate the virulence determinant to help bacteria invade the host and only when a sufficient bacterial cell density has achieved to overwhelm host defense. In this way, there must be something for pathogens to actively sense the host immune status. The authors demonstrate that only in stationary growth phase of Pseudomonas aeruginosa, IFN-g from activated T cell culture could enhance the expression of PA-I lectin and pyocyanin (PCN) which are quorum-sensing dependent virulence determinants, and Rhl quorum-sensing system was also involved. Furthermore, they proved that OprF, the outer membrane protein of Pseudomonas aeruginosa, was the target for IFN-g binding, and only in the wild-type strain treated with IFN-g could we find enhanced expression of PA-I lectin but not in the mutant strains. These results reveal that IFN-g can bind specially to OprF resulting in a quorum-sensing dependent enhancement of PA-I and pyocyanin expression. The observations give not only a highlight for further investigation of quorum-sensing but also a hint to improve the conventional treatment of Pseudomonas aeruginosa infection.

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