FB2025_01 , released February 20, 2025
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Citation
Shinzawa, N., Nelson, B., Aonuma, H., Okado, K., Fukumoto, S., Miura, M., Kanuka, H. (2009). p38 MAPK-dependent phagocytic encapsulation confers infection tolerance in Drosophila.  Cell Host Microbe 6(3): 244--252.
FlyBase ID
FBrf0208827
Publication Type
Research paper
Abstract
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.
PubMed ID
PubMed Central ID
Related Publication(s)
Note

Host tolerance versus resistance and microbial virulence in the host-pathogen equation.
Ferrandon, 2009, Cell Host Microbe 6(3): 203--205 [FBrf0215143]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Cell Host Microbe
    Title
    Cell Host & Microbe
    Publication Year
    2007--
    ISBN/ISSN
    1931-3128 1934-6069
    Data From Reference
    Alleles (9)
    Genes (5)
    Human Disease Models (1)
    Insertions (1)
    Transgenic Constructs (5)