TY - JOUR
T1 - Knockout of mlaA increases Escherichia coli virulence in a silkworm infection model
AU - Nasu, Haruka
AU - Shirakawa, Riko
AU - Furuta, Kazuyuki
AU - Kaito, Chikara
N1 - Funding Information:
This study was supported by JSPS Grants-in-Aid for Scientific Research (grants 19H03466 and 19K22523 [CK]), the Takeda Science Foundation (CK), the Ichiro Kanehara Foundation (CK), and the Ryobi Teien Memory Foundation (CK).The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Funding Information:
Funding:ThisstudywassupportedbyJSPS Grants-in-AidforScientificResearch(grants 19H03466and19K22523[CK]),theTakeda ScienceFoundation(CK),theIchiroKanehara Foundation(CK),andtheRyobiTeienMemory Foundation(CK).Thefundershadnoroleinstudy design,datacollectionandanalysis,decisionto publish,orpreparationofthemanuscript.
Publisher Copyright:
© 2022 Nasu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2022/7
Y1 - 2022/7
N2 - The mlaA gene encodes a lipoprotein to maintain an outer membrane lipid asymmetry in gram-negative bacteria. Although the role of mlaA in bacterial virulence has been studied in several bacterial species, there are no reports of its role in E. coli virulence. In this study, we found that knockout of mlaA in E. coli increased its virulence against silkworms. The mlaA-knockout mutant was sensitive to several antibiotics and detergents, but resistant to vancomycin and chlorhexidine. The mlaA-knockout mutant grew faster than the parent strain in the presence of silkworm hemolymph. The mlaA-knockout mutant also produced a larger amount of outer membrane vesicles than the parent strain. These findings suggest that mlaA knockout causes E. coli resistance to specific antimicrobial substances and increases outer membrane vesicle production, thereby enhancing E. coli virulence properties in the silkworm infection model.
AB - The mlaA gene encodes a lipoprotein to maintain an outer membrane lipid asymmetry in gram-negative bacteria. Although the role of mlaA in bacterial virulence has been studied in several bacterial species, there are no reports of its role in E. coli virulence. In this study, we found that knockout of mlaA in E. coli increased its virulence against silkworms. The mlaA-knockout mutant was sensitive to several antibiotics and detergents, but resistant to vancomycin and chlorhexidine. The mlaA-knockout mutant grew faster than the parent strain in the presence of silkworm hemolymph. The mlaA-knockout mutant also produced a larger amount of outer membrane vesicles than the parent strain. These findings suggest that mlaA knockout causes E. coli resistance to specific antimicrobial substances and increases outer membrane vesicle production, thereby enhancing E. coli virulence properties in the silkworm infection model.
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U2 - 10.1371/journal.pone.0270166
DO - 10.1371/journal.pone.0270166
M3 - Article
C2 - 35830444
AN - SCOPUS:85134289272
SN - 1932-6203
VL - 17
JO - PloS one
JF - PloS one
IS - 7 July
M1 - e0270166
ER -