| Autor: |
John Kevin Collins, John MacSharry, Barry Kiely, Gerald C. O'Sullivan, Liam O'Mahony, Fergus Shanahan, Padraig O'Regan, Austin Powers |
| Rok vydání: |
2003 |
| Předmět: |
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| Zdroj: |
Gastroenterology. 124:A113 |
| ISSN: |
0016-5085 |
| DOI: |
10.1016/s0016-5085(03)80555-3 |
| Popis: |
HB101 HB101 caused little activation of NF-kB. Transformation of HB101 with the EPEC pathogenicity island, locus of enterocyte effacement (LEE), increased NF-kB activation to 72% of EPEC levels. Mutation of key structural TTSS proteins, EspA (UMD872) and EspD (UMD870), decreased NF-kB activation by 34 and 24%, respectively compared to WT. Gene complementation restored NF-kB actwation to levels seen with WT. Mutation of espF (UMD874) decreased NF-kB activation by 59% as compared to WT while complementation of espF restored the phenotype to 80% of WT levels. UMD874 induced virtually no IkBa degradation at 1 hour as compared to 60% for WT, whereas complementation of espF resulted in 83% degradation, lmmunofiuorescent staining of p65 confirmed the nuclear translocation of NF-kB in response to EPEC but not UMD874; this phenotype was restored by espF complementation. RT-PCR was used to evaluate IL-8 mRNA levels. Infection with WT EPEC increased IL8 mRNA levels 1.6 fold over controls. Mutation of espF significantly decreased this response to 125 fold over controls (n=4; p=0.027, WT vs UMD874). Infection with espF complemented UMD874 increased IL-8 mRNA to 1.45 fold over controls which was not significantly different than that in response to WT (n=3; p=0.45). These results indzcate that an effective TTSS and key effector molecules including EspF contribute to EPEC-induced inflammation. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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