The role of JNK signaling in Francisella tularensis infection of Drosophila melanogaster
(English)Manuscript (preprint) (Other academic)
The causative agent of tularemia, Francisella tularensis, inhibits immune signaling pathways during infection and thus reduces the production of proinflammatory cytokines. NF-kB and MAPK pathways are initially activated, but subsequently down-regulated in macrophages. The mechanism(s) of inhibition, or which host proteins that F. tularensis interacts with are not known. Here, we have used Drosophila melanogaster as a genetically amendable model host to study the interaction between F. tularensis LVS and host immune signaling. We found that similar as in mammalian macrophages, LVS inhibits the JNK pathway in flies. LVS interferes with the JNK pathway upstream or at the same level as the JNKK Hemipterous. Expression of an activated Hemipterous in fly macrophage-like cells had a protective effect on fly survival, while inhibiting the JNK pathway in the fly fat body, an important immune tissue, had no effect on fly survival.
Francisella tularensis, LVS, Drosophila melanogaster, JNK, Hemipterous
Microbiology in the medical area
Research subject Clinical Bacteriology
IdentifiersURN: urn:nbn:se:umu:diva-54411OAI: oai:DiVA.org:umu-54411DiVA: diva2:523730