Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria.
Leukocytes in particular CD8+ T cells migration to the brain and parasite sequestration are involved in experimental cerebral malaria (ECM). We hypothesized that ECM is initiated by parasite sequestration in the brain, by adhering to endothelium and/or monocytes or macrophages. Firstly, we assessed...
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| Format: | Final Year Project (FYP) |
| Language: | English |
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2011
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| Online Access: | http://hdl.handle.net/10356/42745 |
| _version_ | 1826114191867510784 |
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| author | Gun, Sin Yee. |
| author2 | School of Biological Sciences |
| author_facet | School of Biological Sciences Gun, Sin Yee. |
| author_sort | Gun, Sin Yee. |
| collection | NTU |
| description | Leukocytes in particular CD8+ T cells migration to the brain and parasite sequestration are involved in experimental cerebral malaria (ECM). We hypothesized that ECM is initiated by parasite sequestration in the brain, by adhering to endothelium and/or monocytes or macrophages. Firstly, we assessed the role of two chemokine receptors CCR2 and CCR5, in leukocyte trafficking to the brain and other organs in ECM and sequestration of infected red blood cells (iRBC). We infected CCR2-deficient mice (50% monocyte reduction) with PbAluc and treated with anti-M-CSF receptor mAb. CCR2-/- treated mice died of ECM with the same parasitemia and parasite biomass as non-treated mice. Next, we investigated the role of CCR5 in ECM. CCR5-deficient mice were as susceptible to ECM as WT mice with no difference in parasitemia and parasite accumulation. Lastly, we investigated the involvement of adhesion molecules (ICAM-1) in iRBC sequestration. Rag2-deficient and C57BL/6J mice treated with anti-ICAM-1 mAb showed an increase in parasitemia with no difference in bioluminescence imaging compared to non-treated mice. These results suggest that iRBC do not adhere to monocytes and/or macrophages; CCR5 is not involved in T cells recruitment; and ICAM-1 might not be the major determinant adhesion molecule during effector phase. |
| first_indexed | 2024-10-01T03:35:29Z |
| format | Final Year Project (FYP) |
| id | ntu-10356/42745 |
| institution | Nanyang Technological University |
| language | English |
| last_indexed | 2024-10-01T03:35:29Z |
| publishDate | 2011 |
| record_format | dspace |
| spelling | ntu-10356/427452023-02-28T18:01:45Z Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. Gun, Sin Yee. School of Biological Sciences A*STAR Singapore Immunology Network Laurent RENIA DRNTU::Science::Biological sciences::Microbiology Leukocytes in particular CD8+ T cells migration to the brain and parasite sequestration are involved in experimental cerebral malaria (ECM). We hypothesized that ECM is initiated by parasite sequestration in the brain, by adhering to endothelium and/or monocytes or macrophages. Firstly, we assessed the role of two chemokine receptors CCR2 and CCR5, in leukocyte trafficking to the brain and other organs in ECM and sequestration of infected red blood cells (iRBC). We infected CCR2-deficient mice (50% monocyte reduction) with PbAluc and treated with anti-M-CSF receptor mAb. CCR2-/- treated mice died of ECM with the same parasitemia and parasite biomass as non-treated mice. Next, we investigated the role of CCR5 in ECM. CCR5-deficient mice were as susceptible to ECM as WT mice with no difference in parasitemia and parasite accumulation. Lastly, we investigated the involvement of adhesion molecules (ICAM-1) in iRBC sequestration. Rag2-deficient and C57BL/6J mice treated with anti-ICAM-1 mAb showed an increase in parasitemia with no difference in bioluminescence imaging compared to non-treated mice. These results suggest that iRBC do not adhere to monocytes and/or macrophages; CCR5 is not involved in T cells recruitment; and ICAM-1 might not be the major determinant adhesion molecule during effector phase. Bachelor of Science in Biomedical Sciences 2011-01-10T04:57:00Z 2011-01-10T04:57:00Z 2010 2010 Final Year Project (FYP) http://hdl.handle.net/10356/42745 en Nanyang Technological University 27 p. application/pdf |
| spellingShingle | DRNTU::Science::Biological sciences::Microbiology Gun, Sin Yee. Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. |
| title | Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. |
| title_full | Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. |
| title_fullStr | Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. |
| title_full_unstemmed | Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. |
| title_short | Involvement of chemokine receptors and adhesion molecules in the regulation of Experimental Cerebral Malaria. |
| title_sort | involvement of chemokine receptors and adhesion molecules in the regulation of experimental cerebral malaria |
| topic | DRNTU::Science::Biological sciences::Microbiology |
| url | http://hdl.handle.net/10356/42745 |
| work_keys_str_mv | AT gunsinyee involvementofchemokinereceptorsandadhesionmoleculesintheregulationofexperimentalcerebralmalaria |