期刊
CELL HOST & MICROBE
卷 6, 期 3, 页码 244-252出版社
CELL PRESS
DOI: 10.1016/j.chom.2009.07.010
关键词
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资金
- Ministry of Health, Labor, and Welfare
- Japanese Ministry of Education, Science, Sports, Culture and Technology
- Astellas Foundation for Research on Metabolic Disorders
- Program for the Promotion of Basic Research Activities for Innovative Biosciences (PROBRAIN)
- Japan Society for the Promotion of Science
Hosts employ a combination of two distinct yet compatible strategies to defend themselves against parasites: resistance, the ability to limit parasite burden, and tolerance, the ability to limit damage caused by a given parasite burden. Animals typically exhibit considerable genetic variation in resistance to a variety of pathogens; however, little is known about whether animals can evolve tolerance. Using a bacterial infection model in Drosophila, we uncovered a p38 MAP kinase-mediated mechanism of tolerance to intracellular bacterial infection as measured by the extent to which the host's survival rate increased or was maintained despite increasing bacterial burden. This increased survival was conferred primarily by a tolerance strategy whereby p38-dependent phagocytic encapsulation of bacteria resulted in enlarged phagocytes that trap bacteria. These results suggest that phagocytic responses are not restricted to resistance mechanisms but can also be applied to tolerance strategies for intracellular encapsulation of pathogens during the invertebrate immune response.
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