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| Author(s): |
Matheus Ferracini
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2009-07-17 |
| Examining board members: |
Sonia Jancar Negro;
José Walber Miranda Costa Cruz;
Paulina Sannomiya
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| Advisor: | Sonia Jancar Negro |
| Abstract | |
We evaluated the role of leukotrienes (LTs), the signaling pathways and the effect of insulin in phagocytosis via FcgR by alveolar macrophages (AMs) from healthy (HR) and diabetic (DR) rats. The results showed that: a) AMs from DR showed lower phagocytic capacity than AMs from healthy rats; b) the phagocytosis was dependent of endogenous LTs in AMs from HR but not DR; c) addition of LTB4 and LTD4 to cultures enhanced the phagocytosis by AMs from HR and DR; d) AMs from HR and DR rats produced similar levels of LTB4 and LTC4; e) addition of insulin to AMs enhanced the phagocytic capacity in HR and DR; f) in HR, the phagocytosis via FcgR induced Akt and PKC-d phosphorylation, which is amplified by endogenous LTs, whereas in DR, only PKC-d was phosphorylated. The phosphorylation of Akt and PKC-d, amplified by LTs produced under FcgR engagement in AMs from HR, seems to be, in a way, dependent of insulin action, because AMs from DR have lower phagocytic capacity, the phagocytosis is not dependent of endogenous LTs and the FcgR engagement is not capable to activate Akt. (AU) | |