期刊
CELL REPORTS
卷 25, 期 7, 页码 1938-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.10.073
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资金
- NIH [R01AI111940, R21A127182, DK59600]
- Bill and Melinda Gates Foundation [OPP1130017]
- UAB Center for AIDS Research (CFAR)
- Center for Free Radical Biology (CFRB)
- South African Medical Research Council
- Bill and Melinda Gates Foundation [OPP1130017] Funding Source: Bill and Melinda Gates Foundation
Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that controls inflammatory responses and redox homeostasis; however, its role during pulmonary tuberculosis (TB) remains unclear. Using freshly resected human TB lung tissue, we examined the role of HO-1 within the cellular and pathological spectrum of TB. Flow cytometry and histopathological analysis of human TB lung tissues showed that HO-1 is expressed primarily in myeloid cells and that HO-1 levels in these cells were directly proportional to cytoprotection. HO-1 mitigates TB pathophysiology by diminishing myeloid cell-mediated oxidative damage caused by reactive oxygen and/or nitrogen intermediates, which control granulocytic karyorrhexis to generate a zonal HO-1 response. Using whole-body or myeloid-specific HO-1-deficient mice, we demonstrate that HO-1 is required to control myeloid cell infiltration and inflammation to protect against TB progression. Overall, this study reveals that zonation of HO-1 in myeloid cells modulates free-radical-mediated stress, which regulates human TB immunopathology.
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