Projects / Programmes
Interactions between Shigella flexneri and components of inflammatory exudate
| Code |
Science |
Field |
Subfield |
| 4.06.02 |
Biotechnical sciences |
Biotechnology |
Bio-engineering |
| Code |
Science |
Field |
| B510 |
Biomedical sciences |
Infections |
| B500 |
Biomedical sciences |
Immunology, serology, transplantation |
Shigellae, flexneri, polymorphonuclear, leukocytes, PMN, inflammation, exudate, macrophage, BPI, membrane, protein secretion, Ipa, apoptois, phagolysosome.
Researchers (3)
| no. |
Code |
Name and surname |
Research area |
Role |
Period |
No. of publicationsNo. of publications |
| 1. |
03156 |
MSc Polonca Čadež |
Biochemistry and molecular biology |
Researcher |
1998 - 1999 |
64 |
| 2. |
17794 |
Simona Leskovec |
|
Researcher |
1998 - 1999 |
25 |
| 3. |
05993 |
PhD Ines Mandić-Mulec |
Biotechnology |
Head |
1998 - 1999 |
639 |
Abstract
Shigellae are intercellular parasites that cause severe dysentery, a disease of considerable public health importance. Its wide dissemination through the epithelium of colonic mucosa is essential to generate abscesses and ulceration, leading to severe inflammation and tissue damage that accounts for clinical manifestation of dysentery. Paradoxically, the inflammatory process, which is largely responsible for the tissue destruction, is ultimately required for the resolution of infection. Ver little is known about the interaction between Shigellae and components of inflammatory exudate. We are studying defense mechanisms involved in resolution of shigellosis using a long - standing model of inflammation, namely, a sterile rabbit peritoneal exudate in which both cellular and extracellular components, characteristic of acute inflammatory exudate, are readily available for study. We have shown that invasive wild type strain of S. flexneri (M90T) and a plasmid cured noninvasive derivative (BS176) are killed by PMN by an oxygen independent mechanism with similar efficiency. Using electron microscopy we have also shown that both strains remain entrapped in the phagolysosome of PMN, which is different from behavior of virulent M90T in macrophages, where virulent Shigellae escape into cytoplasm of these phagocytes and induce their apoptosis. We are now studying the mechanisms responsible for entrapment of S. flexneri in PMN phagolysosomes by testing the hypothesis that proteins present in PMN phagolysosome and especially the bactericidal/permeability-increasing protein (BPI) are responsible for different fate of S. flexneri in PMN. We are most interested whether and how these proteins affect the secretion of S. flexneri specific invasins, namely the Ipa proteins and their type III secretion system.
