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https://scholarbank.nus.edu.sg/handle/10635/27698
DC Field | Value | |
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dc.title | Host innate immunity to Burkholderia pseudomallei infection | |
dc.contributor.author | HII CHUNG SHII | |
dc.date.accessioned | 2011-10-12T18:01:27Z | |
dc.date.available | 2011-10-12T18:01:27Z | |
dc.date.issued | 2008-08-04 | |
dc.identifier.citation | HII CHUNG SHII (2008-08-04). Host innate immunity to Burkholderia pseudomallei infection. ScholarBank@NUS Repository. | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/27698 | |
dc.description.abstract | Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease endemic in Southeast Asia and Northern Australia. The epithelium represents the first cells in contact with bacteria during mucosal infection. Although interaction of B. pseudomallei with epithelial cells has been reported, little is known about its interaction with polarized epithelial cells. We show that B. pseudomallei is able to invade and induce IL-8 secretion in a Type Three Secretion System (TTSS)-dependent but Toll-like receptor (TLR)-independent manner in polarized Caco-2 cells. Using HEK293T cells which is devoid of any TLR, we confirmed this observation and further show that it is independent of intracellular PRR but requires bacterial internalization. Activation of NF-kB and MAPK, JNK are crucial for regulating IL-8 induction. Furthermore, B. pseudomallei can stimulate various TLRs but the activation level is lower compared to a TTSS-deficient mutant, implying that bacteria can suppress TLR-induced NF-kB activation through the TTSS. | |
dc.language.iso | en | |
dc.subject | Burkholderia pseudomallei, NF-kB, MAPK, TLR, Type Three Secretion system, IL-8 | |
dc.type | Thesis | |
dc.contributor.department | BIOCHEMISTRY | |
dc.contributor.supervisor | GAN YUNN HWEN | |
dc.description.degree | Ph.D | |
dc.description.degreeconferred | DOCTOR OF PHILOSOPHY | |
dc.identifier.isiut | NOT_IN_WOS | |
Appears in Collections: | Ph.D Theses (Open) |
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Thesis complete-final correction.pdf | 3.99 MB | Adobe PDF | OPEN | None | View/Download |
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