Complementary immune roles for infected and uninfected cells during bacterial infection (INC7P.425)
| Autor: | Alan Copenhaver, Cierra Casson, Hieu Nguyen, Thomas Fung, Matthew Duda, Craig Roy, Sunny Shin |
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| Rok vydání: | 2014 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 192:186.26-186.26 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.192.supp.186.26 |
| Popis: | The innate immune system responds to virulent pathogens, yet many pathogens manipulate host signaling pathways which should limit immune activation. To understand how the immune system overcomes pathogenic manipulation we study the intracellular bacterium Legionella pneumophila, the cause of the severe pneumonia Legionnaire’s disease. Legionella utilizes a type IV secretion system to inject bacterial proteins into the cytosol of infected cells. Several of these bacterial effector proteins inactivate host cell factors involved in protein translation. Despite Legionella's ability to block host protein translation, inflammatory cytokines are still made against Legionella. It is unclear how infected cells can mount a cytokine response when host protein synthesis is blocked. Our studies demonstrate that infected cells do not produce many cytokines, such as IL-6 and TNF, critical for controlling Legionella infection. Instead, uninfected, bystander cells produce these cytokines. Infected host cells do produce IL-1 de novo. These data suggest that infected cells have mechanisms to overcome protein synthesis inhibition to produce IL-1 and that uninfected, bystander cells are important contributors to the immune response during infection with Legionella. This mechanism of immune activation has broad significance as many other bacterial pathogens manipulate immune cell signaling. |
| Databáze: | OpenAIRE |
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