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- W2442112 startingPage "43.1" @default.
- W2442112 abstract "Abstract M. tuberculosis infects lung macrophages (MØs) and evades immune responses by a diverse array of mechanisms. We have recently published that BCG infection triggers a MyD88-dependent Arg1 induction that suppresses NO production from infected MØs. In addition, MØ-specific Arg1 conditional knockout mice were more efficient at clearing M. tuberculosis and BCG. In the present study, we have found that while MyD88 is essential for Arg1 induction following infection, MyD88-/- MØs express robust Arg1 mRNA and protein when stimulated with supernatant from BCG-infected WT MØs. Arg1 induction stimulated with BCG supernatant correlated with enhanced activation of Stat3, but not Stat1, 4, 5, or 6. Two Stat3 activators, IL-6 and IL-10, were present in the supernatants of BCG infected WT MØs. We found the combined treatment of MØs with IL-6 and IL-10 synergistically induces Arg1 in the presence or absence of BCG infection. Consequently, we propose a model by which Arg1 is induced directly by BCG infection via MyD88 signaling, and indirectly through the autocrine/paracrine IL-6/IL-10 activation of Stat3. These data suggest that mycobacteria can condition uninfected neighboring cells to suppress NO production." @default.
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- W2442112 date "2009-04-01" @default.
- W2442112 modified "2023-10-18" @default.
- W2442112 title "Direct and indirect type-1 arginase (Arg1) induction following <i>Mycobacterium bovis</i> (BCG) infection (43.1)" @default.
- W2442112 doi "https://doi.org/10.4049/jimmunol.182.supp.43.1" @default.
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