Diverse Clinical Isolates of Mycobacterium tuberculosis Develop Macrophage-Induced Rifampin Tolerance

被引：18

作者：

Adams, Kristin N. ^{[1
]}

Verma, Amit Kumar ^{[3
]}

Gopalaswamy, Radha ^{[4
]}

Adikesavalu, Harresh ^{[4
]}

Singhal, Dinesh Kumar ^{[4
]}

Tripathy, Srikanth ^{[4
]}

Ranganathan, Uma Devi ^{[4
]}

Sherman, David R. ^{[1
]}

Urdahl, Kevin B. ^{[1
]}

Ramakrishnan, Lalita ^{[3
]}

Hernandez, Rafael E. ^{[1
,2
]}

机构：

[1] Seattle Childrens Res Inst, Ctr Infect Dis Res, Ctr Global Infect Dis Res, Seattle, WA USA

[2] Univ Washington, Dept Pediat, Seattle, WA 98195 USA

[3] Univ Cambridge, Dept Med, Mol Immun Unit, Cambridge, England

[4] Natl Inst Res TB, Chennai, Tamil Nadu, India

来源：

JOURNAL OF INFECTIOUS DISEASES | 2019年 / 219卷 / 10期

基金：

英国惠康基金; 英国医学研究理事会; 美国国家卫生研究院;

关键词：

Tuberculosis; drug efflux; Beijing lineage; Rv1258c; antibiotic tolerance; TRANSCRIPTIONAL ADAPTATION; IN-VITRO;

D O I：

10.1093/infdis/jiy710

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The Mycobacterium tuberculosis lineage 4 strains CDC1551 and H37Rv develop tolerance to multiple antibiotics upon macrophage residence. To determine whether macrophage-induced tolerance is a general feature of clinical M. tuberculosis isolates, we assessed macrophage-induced drug tolerance in strains from lineages 1-3, representing the other predominant M. tuberculosis strains responsible for tuberculosis globally. All 3 lineages developed isoniazid tolerance. While lineage 1, 3, and 4 strains developed rifampin tolerance, lineage 2 Beijing strains did not. Their failure to develop tolerance may be explained by their harboring of a loss-of-function mutation in the Rv1258c efflux pump that is linked to macrophage-induced rifampicin tolerance.

引用

页码：1554 / 1558

页数：5

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