Open Close
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
Publication Type
Research paper

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)

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

Associated Information
Associated Files
Other Information
Secondary IDs
    Language of Publication
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Cell Host Microbe
    Cell Host & Microbe
    Publication Year
    1931-3128 1934-6069
    Data From Reference
    Alleles (9)
    Genes (5)
    Insertions (1)
    Transgenic Constructs (5)