Early inhibition of mycobacterial growth by human alveolar macrophages is not due to nitric oxide.
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The Role of Nitric Oxide in Mycobacterial InfectionsMycobacteria counteract a TLR-mediated nitrosative defense mechanism in a zebrafish infection modelNeutrophils are the predominant infected phagocytic cells in the airways of patients with active pulmonary TB.Interactions of attenuated Mycobacterium tuberculosis phoP mutant with human macrophages.Induction of inducible nitric oxide synthase-NO* by lipoarabinomannan of Mycobacterium tuberculosis is mediated by MEK1-ERK, MKK7-JNK, and NF-kappaB signaling pathways.Tumor necrosis factor alpha stimulates killing of Mycobacterium tuberculosis by human neutrophils.What is the role of nitric oxide in murine and human host defense against tuberculosis?Current knowledge.Different innate ability of I/St and A/Sn mice to combat virulent Mycobacterium tuberculosis: phenotypes expressed in lung and extrapulmonary macrophages.The Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits gamma interferon-regulated HLA-DR and Fc gamma R1 on human macrophages through Toll-like receptor 2.Serious infections associated with anticytokine therapies in the rheumatic diseases.Virulent but not avirulent Mycobacterium tuberculosis can evade the growth inhibitory action of a T helper 1-dependent, nitric oxide Synthase 2-independent defense in miceAerosolized gamma interferon (IFN-gamma) induces expression of the genes encoding the IFN-gamma-inducible 10-kilodalton protein but not inducible nitric oxide synthase in the lung during tuberculosis.Lysosomal Disorders Drive Susceptibility to Tuberculosis by Compromising Macrophage Migration.Mycobacterium tuberculosis growth control by lung macrophages and CD8 cells from patient contacts.Mitogen-activated protein kinases and NFkappaB are involved in SP-A-enhanced responses of macrophages to mycobacteria.CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis.Epigenetic silencing of the human NOS2 gene: rethinking the role of nitric oxide in human macrophage inflammatory responses.Within the Enemy's Camp: contribution of the granuloma to the dissemination, persistence and transmission of Mycobacterium tuberculosis.In search of a new paradigm for protective immunity to TBSTAT3 Represses Nitric Oxide Synthesis in Human Macrophages upon Mycobacterium tuberculosis Infection.Phenolic Glycolipid Facilitates Mycobacterial Escape from Microbicidal Tissue-Resident Macrophages.Nitric Oxide in the Pathogenesis and Treatment of Tuberculosis.Mycobacterium tuberculosis induces high production of nitric oxide in coordination with production of tumour necrosis factor-alpha in patients with fresh active tuberculosis but not in MDR tuberculosis.Exhaled Nitric Oxide is Not a Biomarker for Pulmonary Tuberculosis.Lung cell responses to M. tuberculosis in genetically susceptible and resistant mice following intratracheal challenge.Sera from patients with active pulmonary tuberculosis and their household contacts induce nuclear changes in neutrophilsModulating Iron for Metabolic Support of TB Host Defense
P2860
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P2860
Early inhibition of mycobacterial growth by human alveolar macrophages is not due to nitric oxide.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh-hant
name
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@en
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@nl
type
label
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@en
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@nl
prefLabel
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@en
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@nl
P2093
P2860
P1476
Early inhibition of mycobacter ...... es is not due to nitric oxide.
@en
P2093
P2860
P304
P356
10.1164/AJRCCM.157.6.9705028
P407
P433
P50
P577
1998-06-01T00:00:00Z