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- W57765684 abstract "Abstract Francisella tularensis is a highly infectious Gram-negative bacterial pathogen and the causative agent of pneumonic tularemia. We recently demonstrated inhibition of F. tularensis LVS replication in macrophages via mast cell production of interleukin-4 (IL-4). We have further analyzed the interactions of mast cells and macrophages using a primary bone marrow derived mast cell-macrophage co-culture system and determined that mast cells inhibit F. tularensis-induced macrophage apoptosis. Specifically, mast cells co-cultured with macrophages significantly reduced intramacrophage LVS growth and expression of apoptotic proteins caspase-3 (19.9%) and PARP (Poly-ADP ribose polymerase, 16.0%) compared to macrophages cultured alone (48.2% and 56.4%, respectively). The inhibition of LVS-induced apoptosis within infected macrophages also was seen by the direct addition of recombinant IL-4 and corresponded with up-regulation of mannose receptor expression and arginase activity which are associated with the alternative activation of macrophages. Moreover, IL4R-/- mice were more susceptible to intranasal challenge and exhibited greater caspase-3 activity in lung macrophages (12.9%) compared to similarly challenged wild-type (4.7%) animals. These results support a role for mast cells and IL-4 in control of bacterial replication and apoptosis following pulmonary LVS infection. National Institutes of Health grant PO1 AI057986; NIH/NIGMS MBRS-RISE GM60655" @default.
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- W57765684 date "2009-04-01" @default.
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- W57765684 title "Mast cells induce alternative activation and inhibit caspase-3 mediated apoptosis of Francisella tularensis infected macrophages (44.24)" @default.
- W57765684 doi "https://doi.org/10.4049/jimmunol.182.supp.44.24" @default.
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