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- W4313382045 abstract "Abstract Infection with M. tuberculosis (Mtb) induces the upregulation of heme oxygenase-1 (HO-1), a powerful antioxidant enzyme that catalyzes the degradation of heme into iron, biliverdin and carbon monoxide. We observed that administration of tin protoporphyrin IX (SnPPIX), a well-characterized HO-1 activity inhibitor, to Mtb-infected mice resulted in pulmonary bacterial load reduction. Moreover, adjunct administration of SnPPIX to Mtb-infected mice receiving antibiotic treatment improved and accelerated pathogen clearance. Interestingly, both the induction of HO-1 expression in lungs of Mtb-infected mice and the efficacy of in vivo SnPPIX-mediated bacterial burden reduction were dependent on the presence of host TCR-α+ lymphocytes as well as IFN-γ suggesting a role for the immune response in the activity of the drug. Further investigation revealed that in the lungs of these immunodeficient mice the numbers of parenchymal CD11b+ myeloid cells staining positive for HO-1 were substantially reduced. SnPPIX treatment of Mtb-infected mouse bone marrow derived macrophages also resulted in diminished bacterial loads in vitro and this effect was reverted by iron supplementation and enhanced by iron chelation. Based on these observations we propose that HO-1 inhibition promotes control of Mtb by limiting the availability of nutrient iron and that the host Th1 response regulates this effect by controlling the recruitment to the lungs of a subset of myeloid cells that is both capable of HO-1 expression and permissive to bacterial infection. This work was supported by the intramural research program of the NIAID." @default.
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- W4313382045 date "2017-05-01" @default.
- W4313382045 modified "2023-09-26" @default.
- W4313382045 title "Inhibition of heme oxygenase-1 activity suppresses <i>Mycobacterium tuberculosis</i> infection <i>in vivo</i> by a mechanism dependent on T lymphocytes and IFN-γ production" @default.
- W4313382045 doi "https://doi.org/10.4049/jimmunol.198.supp.216.7" @default.
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