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Evaluation of the expression of cytokines and chemokines in macrophages in response to rifampin-monoresistant Mycobacterium tuberculosis and H37Rv strain
被引:3
作者:
Ravan, Parvaneh
[1
]
Sattari, Taher Nejad
[1
]
Siadat, Seyed Davar
[2
,3
]
Vaziri, Farzam
[2
,3
]
机构:
[1] Islamic Azad Univ, Dept Biol, Sci & Res Branch, Tehran, Iran
[2] Pasteur Inst Iran, Dept Mycobacteriol & Pulm Res, Tehran 1316943551, Iran
[3] Pasteur Inst Iran, MRC, Tehran, Iran
来源:
关键词:
Rifampin monoresistance;
Mycobacterium tuberculosis;
THP-1;
Cytokines;
Chemokines;
GENE-EXPRESSION;
UP-REGULATION;
RESISTANCE;
CELLS;
ACTIVATION;
INFECTION;
SECRETION;
AUTOPHAGY;
PATHWAY;
INNATE;
D O I:
10.1016/j.cyto.2018.12.004
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Macrophages are the primary phagocytes in the lungs and a part of the host defense system against Mycobacterium tuberculosis (Mtb), involved in the primary immune response. While several studies have assessed the effects of resistance to rifampin on Mtb physiology, the consequences of mutations in genes encoding the beta subunit of RNA polymerase (rpoB) for host-pathogen interactions remain poorly understood. In this study, rifampin-monoresistant (RMR) Mtb and H37Rv strains were used to infect the THP-1-derived macrophages. Realtime quantitative reverse transcription PCR assay was carried out to determine mRNA expression in 84 cytokine and chemokine genes. Production of specific cytokines and chemokines was measured by ELISA assay. In conclusion, the current study shed more light on the fitness cost of RMR strain and the potential effects of rpoB gene mutations on Mtb-host interactions. These results initially demonstrate that the Mtb carrying the rpoB-S450L can modulate macrophage responses to mediate bacterial survival.
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页码:127 / 134
页数:8
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