Mutations in genes lpxL1 , bamA , and pmrB impair the susceptibility of cystic fibrosis strains of Pseudomonas aeruginosa to murepavadin
Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against species. In the present study, its activity was assessed on 230 cystic fibrosis (CF) strains of isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in...
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Published in | Antimicrobial agents and chemotherapy Vol. 68; no. 1; p. e0129823 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Society for Microbiology
10.01.2024
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Abstract | Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against
species. In the present study, its
activity was assessed on 230 cystic fibrosis (CF) strains of
isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in preclinical stage of development, 9.1% (
= 21) of strains had a minimum inhibitory concentration (MIC) >4 mg/L, a level at least 128-fold higher than the modal MIC value of the whole collection (≤0.06 mg/L). Whole-genome sequencing of these 21 strains along with more susceptible isogenic counterparts coexisting in the same patients revealed diverse mutations in genes involved in the synthesis (
and
) or transport of lipopolysaccharides (
,
, and
), or encoding histidine kinases of two-component systems (
and
). Allelic replacement experiments with wild-type reference strain PAO1 confirmed that alteration of genes
,
and/or
can decrease the murepavadin susceptibility from 8- to 32-fold. Furthermore, we found that specific amino acid substitutions in histidine kinase PmrB (G188D, Q105P, and D45E) reduce the susceptibility of
to murepavadin, colistin, and tobramycin, three antibiotics used or intended to be used (murepavadin) in aerosols to treat colonized CF patients. Whether colistin or tobramycin may select mutants resistant to murepavadin or the opposite needs to be addressed by clinical studies. |
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AbstractList | Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against
Pseudomonas
species. In the present study, its
in vitro
activity was assessed on 230 cystic fibrosis (CF) strains of
Pseudomonas aeruginosa
isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in preclinical stage of development, 9.1% (
n
= 21) of strains had a minimum inhibitory concentration (MIC) >4 mg/L, a level at least 128-fold higher than the modal MIC value of the whole collection (≤0.06 mg/L). Whole-genome sequencing of these 21 strains along with more susceptible isogenic counterparts coexisting in the same patients revealed diverse mutations in genes involved in the synthesis (
lpxL1
and
lpxL2
) or transport of lipopolysaccharides (
bamA
,
lptD
, and
msbA
), or encoding histidine kinases of two-component systems (
pmrB
and
cbrA
). Allelic replacement experiments with wild-type reference strain PAO1 confirmed that alteration of genes
lpxL1
,
bamA,
and/or
pmrB
can decrease the murepavadin susceptibility from 8- to 32-fold. Furthermore, we found that specific amino acid substitutions in histidine kinase PmrB (G188D, Q105P, and D45E) reduce the susceptibility of
P. aeruginosa
to murepavadin, colistin, and tobramycin, three antibiotics used or intended to be used (murepavadin) in aerosols to treat colonized CF patients. Whether colistin or tobramycin may select mutants resistant to murepavadin or the opposite needs to be addressed by clinical studies. ABSTRACT Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was assessed on 230 cystic fibrosis (CF) strains of Pseudomonas aeruginosa isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in preclinical stage of development, 9.1% ( n = 21) of strains had a minimum inhibitory concentration (MIC) >4 mg/L, a level at least 128-fold higher than the modal MIC value of the whole collection (≤0.06 mg/L). Whole-genome sequencing of these 21 strains along with more susceptible isogenic counterparts coexisting in the same patients revealed diverse mutations in genes involved in the synthesis ( lpxL1 and lpxL2 ) or transport of lipopolysaccharides ( bamA , lptD , and msbA ), or encoding histidine kinases of two-component systems ( pmrB and cbrA ). Allelic replacement experiments with wild-type reference strain PAO1 confirmed that alteration of genes lpxL1 , bamA, and/or pmrB can decrease the murepavadin susceptibility from 8- to 32-fold. Furthermore, we found that specific amino acid substitutions in histidine kinase PmrB (G188D, Q105P, and D45E) reduce the susceptibility of P. aeruginosa to murepavadin, colistin, and tobramycin, three antibiotics used or intended to be used (murepavadin) in aerosols to treat colonized CF patients. Whether colistin or tobramycin may select mutants resistant to murepavadin or the opposite needs to be addressed by clinical studies. ABSTRACT Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was assessed on 230 cystic fibrosis (CF) strains of Pseudomonas aeruginosa isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in preclinical stage of development, 9.1% ( n = 21) of strains had a minimum inhibitory concentration (MIC) >4 mg/L, a level at least 128-fold higher than the modal MIC value of the whole collection (≤0.06 mg/L). Whole-genome sequencing of these 21 strains along with more susceptible isogenic counterparts coexisting in the same patients revealed diverse mutations in genes involved in the synthesis ( lpxL1 and lpxL2 ) or transport of lipopolysaccharides ( bamA , lptD , and msbA ), or encoding histidine kinases of two-component systems ( pmrB and cbrA ). Allelic replacement experiments with wild-type reference strain PAO1 confirmed that alteration of genes lpxL1 , bamA, and/or pmrB can decrease the murepavadin susceptibility from 8- to 32-fold. Furthermore, we found that specific amino acid substitutions in histidine kinase PmrB (G188D, Q105P, and D45E) reduce the susceptibility of P. aeruginosa to murepavadin, colistin, and tobramycin, three antibiotics used or intended to be used (murepavadin) in aerosols to treat colonized CF patients. Whether colistin or tobramycin may select mutants resistant to murepavadin or the opposite needs to be addressed by clinical studies. Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against species. In the present study, its activity was assessed on 230 cystic fibrosis (CF) strains of isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in preclinical stage of development, 9.1% ( = 21) of strains had a minimum inhibitory concentration (MIC) >4 mg/L, a level at least 128-fold higher than the modal MIC value of the whole collection (≤0.06 mg/L). Whole-genome sequencing of these 21 strains along with more susceptible isogenic counterparts coexisting in the same patients revealed diverse mutations in genes involved in the synthesis ( and ) or transport of lipopolysaccharides ( , , and ), or encoding histidine kinases of two-component systems ( and ). Allelic replacement experiments with wild-type reference strain PAO1 confirmed that alteration of genes , and/or can decrease the murepavadin susceptibility from 8- to 32-fold. Furthermore, we found that specific amino acid substitutions in histidine kinase PmrB (G188D, Q105P, and D45E) reduce the susceptibility of to murepavadin, colistin, and tobramycin, three antibiotics used or intended to be used (murepavadin) in aerosols to treat colonized CF patients. Whether colistin or tobramycin may select mutants resistant to murepavadin or the opposite needs to be addressed by clinical studies. Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was assessed on 230 cystic fibrosis (CF) strains of Pseudomonas aeruginosa isolated from 12 French hospitals, in comparison with 12 other antipseudomonal antibiotics. Although murepavadin is still in preclinical stage of development, 9.1% (n = 21) of strains had a minimum inhibitory concentration (MIC) >4 mg/L, a level at least 128-fold higher than the modal MIC value of the whole collection (≤0.06 mg/L). Whole-genome sequencing of these 21 strains along with more susceptible isogenic counterparts coexisting in the same patients revealed diverse mutations in genes involved in the synthesis (lpxL1 and lpxL2) or transport of lipopolysaccharides (bamA, lptD, and msbA), or encoding histidine kinases of two-component systems (pmrB and cbrA). Allelic replacement experiments with wild-type reference strain PAO1 confirmed that alteration of genes lpxL1, bamA, and/or pmrB can decrease the murepavadin susceptibility from 8- to 32-fold. Furthermore, we found that specific amino acid substitutions in histidine kinase PmrB (G188D, Q105P, and D45E) reduce the susceptibility of P. aeruginosa to murepavadin, colistin, and tobramycin, three antibiotics used or intended to be used (murepavadin) in aerosols to treat colonized CF patients. Whether colistin or tobramycin may select mutants resistant to murepavadin or the opposite needs to be addressed by clinical studies. |
Author | Triponney, Pauline Plésiat, Patrick Ghassani, Aya Bour, Maxime Jeannot, Katy |
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Copyright | Copyright © 2023 American Society for Microbiology. Distributed under a Creative Commons Attribution 4.0 International License Copyright © 2023 American Society for Microbiology. 2023 American Society for Microbiology. |
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Keywords | antimicrobial resistance Pseudomonas aeruginosa murepavadin |
Language | English |
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Snippet | Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against
species. In the present study, its
activity was assessed on 230 cystic fibrosis... Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was assessed... ABSTRACT Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was... ABSTRACT Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was... Murepavadin is a peptidomimetic exhibiting specific inhibitory activity against Pseudomonas species. In the present study, its in vitro activity was assessed... |
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SubjectTerms | Anti-Bacterial Agents - pharmacology Anti-Bacterial Agents - therapeutic use Antimicrobial Chemotherapy Colistin - pharmacology Colistin - therapeutic use Cystic Fibrosis - drug therapy Humans Life Sciences Mechanisms of Resistance Microbial Sensitivity Tests Mutation - genetics Pseudomonas aeruginosa Pseudomonas Infections - complications Pseudomonas Infections - drug therapy Respiratory Aerosols and Droplets Tobramycin - pharmacology |
Title | Mutations in genes lpxL1 , bamA , and pmrB impair the susceptibility of cystic fibrosis strains of Pseudomonas aeruginosa to murepavadin |
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