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| Author(s): |
Juliana Mota Khalil Amhaz
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Conjunto das Químicas (IQ e FCF) (CQ/DBDCQ) |
| Defense date: | 2007-08-03 |
| Examining board members: |
Marina Baquerizo Martinez;
Ana Campa;
Rita de Cássia Ruiz;
Rosa Maria Silva;
Carlos Pelleschi Taborda
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| Advisor: | Marina Baquerizo Martinez; Sandro Rogerio de Almeida |
| Abstract | |
During an infection, a complex sequence of events in iniciated after invasion of the host by pathogenic microorganisms. Enteroinvasive Escherichia coli (EIEC) and Shigella cause dysentery by means of invading the colonic mucosa, leading to tissue destruction and inflammation. In arder for an infectious process to occur, inocula of 102 Shigella are necessary incontrast to e 106 EIEC. The infection of J774 macrophages by EIEC resulted in phagocytosis of the bacterium, a hindering of the viability of the macrophage and in the production of cytokines. Macrophages obtained from C57BU6 mice infected with EIEC produced NO, which seems to be important for the control if infection. We observed that in iNOS knockout mice, both the production of proinflammatory cytokines and lethality were higher than that observed in wild-type mice. EIEC induced the migration of granulocytes and monocytes to the peritoneum as well as the secretion of cytokines by these cells. We observed a proliferation of Iymphocytes in response to inoculation with soluble EIEC antigens, however, in this case, the production of cytokines was not detected. Compared to Shigella, EIEC was slower in escaping from the macrophage, and induced a shyer production of pro-inflammatory cytokines and NO, as well as promoted a smaller activation of T Iymphocytes. These data suggest that when challenged with EIEC, the host produces a less severe response than that elicited by Shigella, which might explain why the infectious process with EIEC produces a milder form of dysentery with a quicker resolution. (AU) | |