In this section
@article{Stapels:2018:10.1126/science.aat7148,
author = {Stapels, DAC and Hill, PWS and Westermann, AJ and Fisher, RA and Thurston, TL and Saliba, A-E and Blommestein, I and Vogel, J and Helaine, S},
doi = {10.1126/science.aat7148},
journal = {Science},
pages = {1156--1160},
title = {Salmonella persisters undermine host immune defenses during antibiotic treatment},
url = {http://dx.doi.org/10.1126/science.aat7148},
volume = {362},
year = {2018}
}
TY - JOUR
AB - Many bacterial infections are hard to treat and tend to relapse, possibly due to the presence of antibiotic-tolerant persisters. In vitro, persister cells appear to be dormant. After uptake of Salmonella species by macrophages, nongrowing persisters also occur, but their physiological state is poorly understood. In this work, we show that Salmonella persisters arising during macrophage infection maintain a metabolically active state. Persisters reprogram macrophages by means of effectors secreted by the Salmonella pathogenicity island 2 type 3 secretion system. These effectors dampened proinflammatory innate immune responses and induced anti-inflammatory macrophage polarization. Such reprogramming allowed nongrowing Salmonella cells to survive for extended periods in their host. Persisters undermining host immune defenses might confer an advantage to the pathogen during relapse once antibiotic pressure is relieved.
AU - Stapels,DAC
AU - Hill,PWS
AU - Westermann,AJ
AU - Fisher,RA
AU - Thurston,TL
AU - Saliba,A-E
AU - Blommestein,I
AU - Vogel,J
AU - Helaine,S
DO - 10.1126/science.aat7148
EP - 1160
PY - 2018///
SN - 0036-8075
SP - 1156
TI - Salmonella persisters undermine host immune defenses during antibiotic treatment
T2 - Science
UR - http://dx.doi.org/10.1126/science.aat7148
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000452506300057&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - https://science.sciencemag.org/content/362/6419/1156/
UR - http://hdl.handle.net/10044/1/67905
VL - 362
ER -
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