The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity.
The innate immune system of Anopheles gambiae mosquitoes limits Plasmodium infection through multiple molecular mechanisms. For example, midgut invasion by the parasite triggers an epithelial nitration response that promotes activation of the complement-like system. We found that suppression of the...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS Pathogens |
| Online Access: | http://europepmc.org/articles/PMC3764222?pdf=render |
| _version_ | 1818611190325051392 |
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| author | Lindsey S Garver Giselle de Almeida Oliveira Carolina Barillas-Mury |
| author_facet | Lindsey S Garver Giselle de Almeida Oliveira Carolina Barillas-Mury |
| author_sort | Lindsey S Garver |
| collection | DOAJ |
| description | The innate immune system of Anopheles gambiae mosquitoes limits Plasmodium infection through multiple molecular mechanisms. For example, midgut invasion by the parasite triggers an epithelial nitration response that promotes activation of the complement-like system. We found that suppression of the JNK pathway, by silencing either Hep, JNK, Jun or Fos expression, greatly enhanced Plasmodium infection; while overactivating this cascade, by silencing the suppressor Puckered, had the opposite effect. The JNK pathway limits infection via two coordinated responses. It induces the expression of two enzymes (HPx2 and NOX5) that potentiate midgut epithelial nitration in response to Plasmodium infection and regulates expression of two key hemocyte-derived immune effectors (TEP1 and FBN9). Furthermore, the An. gambiae L3-5 strain that has been genetically selected to be refractory (R) to Plasmodium infection exhibits constitutive overexpression of genes from the JNK pathway, as well as midgut and hemocyte effector genes. Silencing experiments confirmed that this cascade mediates, to a large extent, the drastic parasite elimination phenotype characteristic of this mosquito strain. In sum, these studies revealed the JNK pathway as a key regulator of the ability of An. gambiae mosquitoes to limit Plasmodium infection and identified several effector genes mediating these responses. |
| first_indexed | 2024-12-16T15:26:23Z |
| format | Article |
| id | doaj.art-4801f003db7a43d5a06c7c2af38ffc0c |
| institution | Directory Open Access Journal |
| issn | 1553-7366 1553-7374 |
| language | English |
| last_indexed | 2024-12-16T15:26:23Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Pathogens |
| spelling | doaj.art-4801f003db7a43d5a06c7c2af38ffc0c2022-12-21T22:26:29ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742013-01-0199e100362210.1371/journal.ppat.1003622The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity.Lindsey S GarverGiselle de Almeida OliveiraCarolina Barillas-MuryThe innate immune system of Anopheles gambiae mosquitoes limits Plasmodium infection through multiple molecular mechanisms. For example, midgut invasion by the parasite triggers an epithelial nitration response that promotes activation of the complement-like system. We found that suppression of the JNK pathway, by silencing either Hep, JNK, Jun or Fos expression, greatly enhanced Plasmodium infection; while overactivating this cascade, by silencing the suppressor Puckered, had the opposite effect. The JNK pathway limits infection via two coordinated responses. It induces the expression of two enzymes (HPx2 and NOX5) that potentiate midgut epithelial nitration in response to Plasmodium infection and regulates expression of two key hemocyte-derived immune effectors (TEP1 and FBN9). Furthermore, the An. gambiae L3-5 strain that has been genetically selected to be refractory (R) to Plasmodium infection exhibits constitutive overexpression of genes from the JNK pathway, as well as midgut and hemocyte effector genes. Silencing experiments confirmed that this cascade mediates, to a large extent, the drastic parasite elimination phenotype characteristic of this mosquito strain. In sum, these studies revealed the JNK pathway as a key regulator of the ability of An. gambiae mosquitoes to limit Plasmodium infection and identified several effector genes mediating these responses.http://europepmc.org/articles/PMC3764222?pdf=render |
| spellingShingle | Lindsey S Garver Giselle de Almeida Oliveira Carolina Barillas-Mury The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity. PLoS Pathogens |
| title | The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity. |
| title_full | The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity. |
| title_fullStr | The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity. |
| title_full_unstemmed | The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity. |
| title_short | The JNK pathway is a key mediator of Anopheles gambiae antiplasmodial immunity. |
| title_sort | jnk pathway is a key mediator of anopheles gambiae antiplasmodial immunity |
| url | http://europepmc.org/articles/PMC3764222?pdf=render |
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