BibTex format
@article{Giraud-Gatineau:2020:10.7554/eLife.55692,
author = {Giraud-Gatineau, A and Coya, JM and Maure, A and Biton, A and Thomson, M and Bernard, EM and Marrec, J and Gutierrez, MG and Larrouy-Maumus, G and Brosch, R and Gicquel, B and Tailleux, L},
doi = {10.7554/eLife.55692},
journal = {eLife},
title = {The antibiotic bedaquiline activates host macrophage innate immune resistance to bacterial infection},
url = {http://dx.doi.org/10.7554/eLife.55692},
volume = {9},
year = {2020}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Antibiotics are widely used in the treatment of bacterial infections. Although known for their microbicidal activity, antibiotics may also interfere with the host's immune system. Here, we analyzed the effects of bedaquiline (BDQ), an inhibitor of the mycobacterial ATP synthase, on human macrophages. Genome-wide gene expression analysis revealed that BDQ reprogramed cells into potent bactericidal phagocytes. We found that 579 and 1,495 genes were respectively differentially expressed in naive- and M. tuberculosis-infected macrophages incubated with the drug, with an over-representation of lysosome-associated genes. BDQ treatment triggered a variety of antimicrobial defense mechanisms, including phagosome-lysosome fusion, and autophagy. These effects were associated with activation of transcription factor EB, involved in the transcription of lysosomal genes, resulting in enhanced intracellular killing of different bacterial species that were naturally insensitive to BDQ. Thus, BDQ could be used as a host-directed therapy against a wide range of bacterial infections.
AU - Giraud-Gatineau,A
AU - Coya,JM
AU - Maure,A
AU - Biton,A
AU - Thomson,M
AU - Bernard,EM
AU - Marrec,J
AU - Gutierrez,MG
AU - Larrouy-Maumus,G
AU - Brosch,R
AU - Gicquel,B
AU - Tailleux,L
DO - 10.7554/eLife.55692
PY - 2020///
SN - 2050-084X
TI - The antibiotic bedaquiline activates host macrophage innate immune resistance to bacterial infection
T2 - eLife
UR - http://dx.doi.org/10.7554/eLife.55692
UR - https://www.ncbi.nlm.nih.gov/pubmed/32369020
UR - http://hdl.handle.net/10044/1/79159
VL - 9
ER -
