scholarly journals Competition in biofilms between cystic fibrosis isolates ofPseudomonas aeruginosais shaped by R-pyocins

2018 ◽  
Author(s):  
Olubukola Oluyombo ◽  
Christopher N. Penfold ◽  
Stephen P. Diggle
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Species Interactions ◽  
Clinical Problem ◽  
Opportunistic Pathogen ◽  
Resistance Mechanisms ◽  
Global Concern ◽  
Human Infections ◽  
Antibiofilm Agents

ABSTRACTPseudomonas aeruginosais an opportunistic pathogen responsible for a number of different human infections and is the leading cause of morbidity and mortality in cystic fibrosis (CF) patients.P. aeruginosainfections are difficult to treat due to a number of antibiotic resistance mechanisms and the organisms propensity to form multicellular biofilms. Epidemic strains ofP. aeruginosaoften dominate within the lungs of individual CF patients, but how they achieve this is poorly understood. One of the ways strains ofP. aeruginosacan compete, is by producing chromosomally encoded bacteriocins, called pyocins. Three major classes of pyocin have been identified inP. aeruginosa:soluble pyocins (S-types) and tailocins (R- and F-types). In this study, we investigated the distribution of S- and R-type pyocins in 24 clinical strains isolated from individual CF patients and then focused on understanding their roles on inter-strain competition. We found that (i) each strain produced only one R-pyocin type, but the number of S-pyocins varied between strains; (ii) R-pyocins were generally important for strain dominance during competition assays in planktonic cultures and biofilm communities in strains with both disparate R and S pyocin sub-types. (iii) purified R-pyocins demonstrated significant antimicrobial activity against established biofilms. Our work provides support for a key role played by R-pyocins in the competition betweenP. aeruginosastrains, and may help explain why certain strains and lineages ofP. aeruginosadominate and displace others during CF lung infection. Furthermore, we demonstrate the potential of exploiting R-pyocins for therapeutic gains in an era when antibiotic resistance is a global concern.IMPORTANCEA major clinical problem caused byPseudomonas aeruginosa, is chronic biofilm infection of the lungs in individuals with cystic fibrosis (CF). EpidemicP. aeruginosastrains dominate and displace others during CF infection, but these intra-species interactions remain poorly understood. Here we demonstrate that R-pyocins (bacterocins) are important factors in driving competitive interactions in biofilms betweenP. aeruginosastrains isolated from different CF patients. In addition, we found that these phage-like pyocins are inhibitory against mature biofilms of susceptible strains. This highlights the potential of R-pyocins as antimicrobial and antibiofilm agents, at a time when new antimicrobial therapies are desperately needed.

scholarly journals Competition in Biofilms between Cystic Fibrosis Isolates ofPseudomonas aeruginosaIs Shaped by R-Pyocins

mBio ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. e01828-18 ◽  
Author(s):  
Olubukola Oluyombo ◽  
Christopher N. Penfold ◽  
Stephen P. Diggle
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Clinical Problem ◽  
Opportunistic Pathogen ◽  
Resistance Mechanisms ◽  
Content Type ◽  
Global Concern ◽  
Antibiofilm Agents ◽  
Major Clinical Problem

ABSTRACTPseudomonas aeruginosais an opportunistic pathogen and the leading cause of morbidity and mortality in cystic fibrosis (CF) patients.P. aeruginosainfections are difficult to treat due to a number of antibiotic resistance mechanisms and the organism’s propensity to form multicellular biofilms. Epidemic strains ofP. aeruginosaoften dominate within the lungs of individual CF patients, but how they achieve this is poorly understood. One way that strains ofP. aeruginosacan compete is by producing chromosomally encoded bacteriocins, called pyocins. Three major classes of pyocin have been identified inP. aeruginosa: soluble pyocins (S types) and tailocins (R and F types). In this study, we investigated the distribution of S- and R-type pyocins in 24 clinical strains isolated from individual CF patients and then focused on understanding their roles in interstrain competition. We found that (i) each strain produced only one R-pyocin type, but the number of S-pyocins varied between strains, (ii) R-pyocins were generally important for strain dominance during competition assays in planktonic cultures and biofilm communities in strains with both disparate R- and S-pyocin subtypes, and (iii) purified R-pyocins demonstrated significant antimicrobial activity against established biofilms. Our work provides support for a role played by R-pyocins in the competition betweenP. aeruginosastrains and helps explain why certain strains and lineages ofP. aeruginosadominate and displace others during CF infection. Furthermore, we demonstrate the potential of exploiting R-pyocins for therapeutic gains in an era when antibiotic resistance is a global concern.IMPORTANCEA major clinical problem caused byPseudomonas aeruginosa, is chronic biofilm infection of the lungs in individuals with cystic fibrosis (CF). EpidemicP. aeruginosastrains dominate and displace others during CF infection, but these intraspecies interactions remain poorly understood. Here we demonstrate that R-pyocins (bacteriocins) are important factors in driving competitive interactions in biofilms betweenP. aeruginosastrains isolated from different CF patients. In addition, we found that these phage-like pyocins are inhibitory against mature biofilms of susceptible strains. This highlights the potential of R-pyocins as antimicrobial and antibiofilm agents at a time when new antimicrobial therapies are desperately needed.

Detection of Virulence Factors and Antibiotic Resistance Pattern of Clinical and Intensive Care Unit Environmental Isolates of Pseudomonas aeruginosa

2020 ◽  
Vol 20 (5) ◽  
pp. 758-762
Author(s):  
Omid Zarei ◽  
Hassan Mahmoudi ◽  
Ali Mohammadi Bardbari ◽  
Pezhman Karami ◽  
Mohammad Yousef Alikhani
Keyword(s):  
Intensive Care Unit ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Intensive Care ◽  
Virulence Factors ◽  
Opportunistic Pathogen ◽  
Diffusion Method ◽  
Resistance Pattern ◽  
Disk Diffusion Method ◽  
Human Infections

Background: Pseudomonas aeruginosa is a gram-negative non-glucose fermenting aerobic bacteria and an opportunistic pathogen in humans and animals. The present study was carried out to investigate the distribution of virulence factors and antibiotic resistance properties of P. aeruginosa isolated from patients and intensive care unit (ICU) environment. Material and Methods: A total of 116 P. aeruginosa isolated from patients and ICU environment were collected from Besat hospital in Hamadan, the West of Iran. P. aeruginosa isolates were analyzed based on the presence of the virulence factors encoding genes included exoA, exoS, exoU, and algD using polymerase chain reaction (PCR). Antimicrobial susceptibility test was performed using a disk diffusion method. Results: The results showed the prevalence of exoA 33 (56.9%), exoS 21 (36.20%), exoU 37 (63.8%), and algD 35 (60.34%) genes in ICU environment P. aeruginosa strains and exo A 23 (39.25%), exoS 25 (43.1%), exoU 40(68.98%), and algD 25 (43.1%) genes in clinical isolates of P. aeruginosa. High resistance levels of the clinical and ICU environment isolate to ampicillinsulbactam (100%), were also observed. Conclusions: Our findings should raise awareness about antibiotic resistance in hospitalized patients in Iran. Clinicians should exercise caution in prescribing antibiotics, especially in cases of human infections.

scholarly journals Hypermutator Pseudomonas aeruginosa exploits multiple genetic pathways to develop multidrug resistance during long-term infections in the airways of cystic fibrosis patients

2019 ◽  
Author(s):  
C.A. Colque ◽  
A.G. Albarracín Orio ◽  
S. Feliziani ◽  
R.L. Marvig ◽  
A.R. Tobares ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Multidrug Resistance ◽  
Chronic Infection ◽  
Antibiotic Resistance Genes ◽  
Resistance Mechanisms ◽  
Multi Drug Resistance ◽  
Genetic Pathways ◽  
Resistance Evolution

ABSTRACTPseudomonas aeruginosa exploits intrinsic and acquired resistance mechanisms to resist almost every antibiotic used in chemotherapy. Antimicrobial resistance in P. aeruginosa isolated from cystic fibrosis (CF) patients is further enhanced by the occurrence of hypermutator strains, a hallmark of chronic CF infections. However, the within-patient genetic diversity of P. aeruginosa populations related to antibiotic resistance remains unexplored. Here, we show the evolution of the mutational resistome profile of a P. aeruginosa hypermutator lineage by performing longitudinal and transversal analyses of isolates collected from a CF patient throughout 20 years of chronic infection. Our results show the accumulation of thousands of mutations with an overall evolutionary history characterized by purifying selection. However, mutations in antibiotic resistance genes appear to be positively selected, driven by antibiotic treatment. Antibiotic resistance increased as infection progressed towards the establishment of a population constituted by genotypically diversified coexisting sub-lineages, all of which converged to multi-drug resistance. These sub-lineages emerged by parallel evolution through distinct evolutionary pathways, which affected genes of the same functional categories. Interestingly, ampC and fstI, encoding the β-lactamase and penicillin-binding protein 3, respectively, were found among the most frequently mutated genes. In fact, both genes were targeted by multiple independent mutational events, which led to a wide diversity of coexisting alleles underlying β-lactam resistance. Our findings indicate that hypermutators, apart from boosting antibiotic resistance evolution by simultaneously targeting several genes, favor the emergence of adaptive innovative alleles by clustering beneficial/compensatory mutations in the same gene, hence expanding P. aeruginosa strategies for persistence.IMPORTANCEBy increasing mutation rates, hypermutators boost antibiotic resistance evolution by enabling bacterial pathogens to fully exploit their genetic potential and achieve resistance mechanisms for almost every known antimicrobial agent. Here, we show how co-existing clones from a P. aeruginosa hypermutator lineage that evolved during 20 years of chronic infection and antibiotic chemotherapy, converged to multidrug resistance by targeting genes from alternative genetic pathways that are part of the broad P. aeruginosa resistome. Within this complex assembly of combinatorial genetic changes, in some specific cases, multiple mutations are needed in the same gene to reach a fine tuned resistance phenotype. Hypermutability enables this genetic edition towards higher resistance profiles by recurrently targeting these genes, thus promoting new epistatic relationships and the emergence of innovative resistance-conferring alleles. Our findings help to understand this link between hypermutability and antibiotic resistance, a key challenge for the design of new therapeutic strategies.

Clinical Implications of Pseudomonas aeruginosa: Antibiotic Resistance, Phage & Antimicrobial Peptide Therapy

2019 ◽  
Vol 13 (01) ◽  
pp. 65-86 ◽  
Author(s):  
Wee Siang Lim ◽  
Pooi Leng Ho ◽  
Sam Fong-Yau Li ◽  
Dave Siak-Wei Ow
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Antimicrobial Peptide ◽  
Major Gene ◽  
Opportunistic Pathogen ◽  
Resistance Mechanisms ◽  
Clinical Implications ◽  
Variant Form ◽  
Alternative Treatment Strategy ◽  
Conventional Antibiotics

Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen that is found ubiquitously in the environment. It is also the cause of nosocomial infections, which affects patients with cystic fibrosis (CF) and cathether-related infections. Treatment and eradication of P. aeruginosa is an uphill task as it has already developed resistance to many commonly used antibiotics. Some of the resistance mechanisms that P. aeruginosa employ are having low cell wall permeability, developing efflux system to pump antibiotics out, producing enzymes to inactivate antibiotics, modifying antibiotic targets, forming biofilm as a protection layer against antibiotics, and turning into more pathogenic small colony variant form. In addition, P. aeruginosa uses a host of signaling mechanisms, such as secretion system and quorum sensing, to aid its virulence. With numerous resistance mechanisms developed against conventional antibiotics, new strategies to treat P. aeruginosa infection are required. Bacteriophages such as natural bacteria viruses and studies have suggested that they can be used as an alternative to antibiotics for treatment against P. aeruginosa infections. However, phage therapy also shares the same problem with that of antibiotics, i.e., the development and emergence of bacteria resistance by masking or altering surface recognition features, inhibiting phage DNA injection and employing abortive infection (Abi) system. Another alternative treatment strategy is to use antimicrobial peptides, which are small cationic peptides that are naturally found in most organisms’ immune system. These peptides disrupt cell membrane and key cellular processes, which requires major gene alteration if evasion is needed. Hence, lowering likelihood of resistance development. This paper aims to review our current understanding of the clinical implications of P. aeruginosa infections, the mechanisms of antibiotic resistance, phage-inspired and antimicrobial peptide approaches for treatment of P. aeruginosa infections.

Activities of Tobramycin and Six Other Antibiotics against Pseudomonas aeruginosa Isolates from Patients with Cystic Fibrosis

1999 ◽  
Vol 43 (12) ◽  
pp. 2877-2880 ◽  
Author(s):  
Ribhi M. Shawar ◽  
David L. MacLeod ◽  
Richard L. Garber ◽  
Jane L. Burns ◽  
Jenny R. Stapp ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antimicrobial Agents ◽  
Active Drug ◽  
Resistance Mechanisms ◽  
Phase Iii ◽  
In Vitro Activity ◽  
Phase Iii Clinical Trials ◽  
Multiple Antibiotics

ABSTRACT The in vitro activity of tobramycin was compared with those of six other antimicrobial agents against 1,240 Pseudomonas aeruginosa isolates collected from 508 patients with cystic fibrosis during pretreatment visits as part of the phase III clinical trials of tobramycin solution for inhalation. The tobramycin MIC at which 50% of isolates are inhibited (MIC50) and MIC90 were 1 and 8 μg/ml, respectively. Tobramycin was the most active drug tested and also showed good activity against isolates resistant to multiple antibiotics. The isolates were less frequently resistant to tobramycin (5.4%) than to ceftazidime (11.1%), aztreonam (11.9%), amikacin (13.1%), ticarcillin (16.7%), gentamicin (19.3%), or ciprofloxacin (20.7%). For all antibiotics tested, nonmucoid isolates were more resistant than mucoid isolates. Of 56 isolates for which the tobramycin MIC was ≥16 μg/ml and that were investigated for resistance mechanisms, only 7 (12.5%) were shown to possess known aminoglycoside-modifying enzymes; the remaining were presumably resistant by an incompletely understood mechanism often referred to as “impermeability.”

scholarly journals Growing Menace of Antibacterial Resistance in Clinical Isolates ofPseudomonas aeruginosain Nepal: An Insight of Beta-Lactamase Production

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Shamshul Ansari ◽  
Rabindra Dhital ◽  
Sony Shrestha ◽  
Sangita Thapa ◽  
Ram Puri ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Opportunistic Pathogen ◽  
Resistance Rate ◽  
Diffusion Method ◽  
Beta Lactamase ◽  
Beta Lactam ◽  
Beta Lactam Antibiotics ◽  
Microbiological Methods ◽  
Immunosuppressed Patients

Introduction. Pseudomonas aeruginosais the most frequently isolated organism as it acts as the opportunistic pathogen and can cause infections in immunosuppressed patients. The production of different types of beta-lactamases renders this organism resistant to many commonly used antimicrobials. Therefore, the aim of this study was to document the antibiotic resistance rate inPseudomonas aeruginosaisolated from different clinical specimens.Methods. Pseudomonas aeruginosarecovered was identified by standard microbiological methods. Antibiotic susceptibility testing was performed by modified Kirby-Bauer disc diffusion method following Clinical and Laboratory Standard Institute (CLSI) guidelines and all the suspected isolates were tested for the production of ESBLs, MBLs, and AmpC.Results.Out of total (178) isolates, 83.1% were recovered from the inpatient department (IPD). Majority of the isolates mediated resistance towards the beta-lactam antibiotics, while nearly half of the isolates were resistant to ciprofloxacin. Most of the aminoglycosides used showed resistance rate up to 75% but amikacin proved to be better option. No resistance to polymyxin was observed. ESBLs, MBLs, and AmpC mediated resistance was seen in 33.1%, 30.9%, and 15.7% isolates, respectively.Conclusions. Antibiotic resistance rate and beta-lactamase mediated resistance were high. Thus, regular surveillance of drug resistance is of utmost importance.

scholarly journals Heterogenous response to R-pyocin killing in populations of Pseudomonas aeruginosa sourced from cystic fibrosis lungs

2020 ◽  
Author(s):  
Madeline Mei ◽  
Jacob Thomas ◽  
Stephen P. Diggle
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Genotypic Diversity ◽  
Opportunistic Pathogen ◽  
Chronic Infections ◽  
Bacterial Populations ◽  
Heterogeneous Populations ◽  
Lung Infections ◽  
The Impact ◽  
Lps Binding

AbstractBacteriocins are proteinaceous antimicrobials produced by bacteria which are active against other strains of the same species. R-type pyocins are phage tail-like bacteriocins produced by Pseudomonas aeruginosa. Due to their anti-pseudomonal activity, R-pyocins have potential as therapeutics in infection. P. aeruginosa is a Gram-negative opportunistic pathogen and is particularly problematic for individuals with cystic fibrosis (CF). P. aeruginosa from CF lung infections develop increasing resistance to antibiotics, making new treatment approaches essential. P. aeruginosa populations become phenotypically and genotypically diverse during infection, however little is known of the efficacy of R-pyocins against heterogeneous populations. R-pyocins vary by subtype (R1-R5), distinguished by binding to different residues on the lipopolysaccharide (LPS). Each type varies in killing spectrum, and each strain produces only one R-type. To evaluate the prevalence of different R-types, we screened P. aeruginosa strains from the International Pseudomonas Consortium Database (IPCD) and from our biobank of CF strains. We found that (i) R1-types were the most prevalent R-type among strains from respiratory sources and (ii) isolates collected from the same patient have the same R-type. We then assessed the impact of diversity on R-pyocin susceptibility and found a heterogenous response to R-pyocins within populations, likely due to differences in the LPS core. Our work reveals that heterogeneous populations of microbes exhibit variable susceptibility to R-pyocins and highlights that there is likely heterogeneity in response to other types of LPS-binding antimicrobials, including phage.ImportanceR-pyocins have potential as alternative therapeutics against Pseudomonas aeruginosa in chronic infection, however little is known about the efficacy of R-pyocins in heterogeneous bacterial populations. P. aeruginosa is known to become resistant to multiple antibiotics, as well as evolve phenotypic and genotypic diversity over time; thus it is particularly difficult to eradicate in chronic cystic fibrosis (CF) lung infections. In this study, we found that P. aeruginosa populations from CF lungs maintain the same R-pyocin genotype but exhibit heterogeneity in susceptibility to R-pyocins from other strains. Our findings suggest there is likely heterogeneity in response to other types of LPS-binding antimicrobials, such as phage, highlighting the necessity of further studying the potential of LPS-binding antimicrobial particles as alternative therapies in chronic infections.

Reservoirs of resistance: polymyxin resistance in veterinary-associated companion animal isolates of Pseudomonas aeruginosa

2019 ◽  
Vol 185 (7) ◽  
pp. 206-206 ◽  
Author(s):  
Andrea Scott ◽  
Sian Pottenger ◽  
Dorina Timofte ◽  
Matthew Moore ◽  
Laura Wright ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Pathogenic Bacteria ◽  
Inhibitory Concentration ◽  
Respiratory Infections ◽  
Companion Animals ◽  
Opportunistic Pathogen ◽  
Polymyxin B ◽  
Potential Reservoir ◽  
Human Infections ◽  
Animal Isolates

BackgroundPseudomonas aeruginosa is an opportunistic pathogen and a major cause of infections. Widespread resistance in human infections are increasing the use of last resort antimicrobials such as polymyxins. However, these have been used for decades in veterinary medicine. Companion animals are an understudied source of antimicrobial resistant P. aeruginosa isolates. This study evaluated the susceptibility of P. aeruginosa veterinary isolates to polymyxins to determine whether the veterinary niche represents a potential reservoir of resistance genes for pathogenic bacteria in both animals and humans.Methods and resultsClinical P. aeruginosa isolates (n=24) from UK companion animals were compared for antimicrobial susceptibility to a panel of human-associated isolates (n=37). Minimum inhibitory concentration (MIC) values for polymyxin B and colistin in the companion animals was significantly higher than in human isolates (P=0.033 and P=0.013, respectively). Genotyping revealed that the veterinary isolates were spread throughout the P. aeruginosa population, with shared array types from human infections such as keratitis and respiratory infections, suggesting the potential for zoonotic transmission. Whole genome sequencing revealed mutations in genes associated with polymyxin resistance and other antimicrobial resistance-related genes.ConclusionThe high levels of resistance to polymyxin shown here, along with genetic similarities between some human and animal isolates, together suggest a need for sustained surveillance of this veterinary niche as a potential reservoir for resistant, clinically relevant bacteria in both animals and humans.

scholarly journals Complete Genome Sequence of Pseudomonas aeruginosa Strain AA2 (LMG 27630), an Early Isolate Recovered from the Airway of a German Cystic Fibrosis Patient

2020 ◽  
Vol 9 (26) ◽  
Author(s):  
Andrea Sass ◽  
Tom Coenye
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Respiratory Tract ◽  
Cystic Fibrosis Patient ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Opportunistic Pathogen ◽  
Content Type ◽  
Airway Infections ◽  
Early Isolate

ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that is able to cause various infections, including airway infections in cystic fibrosis patients. Here, we present the complete closed and annotated genome sequence of P. aeruginosa AA2, an isolate obtained early during infection of the respiratory tract of a German cystic fibrosis patient.

scholarly journals Fis Contributes to Resistance of Pseudomonas aeruginosa to Ciprofloxacin by Regulating Pyocin Synthesis

2020 ◽  
Vol 202 (11) ◽  
Author(s):  
Yuqing Long ◽  
Weixin Fu ◽  
Su Wang ◽  
Xuan Deng ◽  
Yongxin Jin ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Bacterial Resistance ◽  
Global Gene Expression ◽  
Chronic Infections ◽  
Mobility Shift ◽  
Content Type ◽  
Regulatory Pathways ◽  
Opportunistic Pathogenic

ABSTRACT Factor for inversion stimulation (Fis) is a versatile DNA binding protein that plays an important role in coordinating bacterial global gene expression in response to growth phases and environmental stresses. Previously, we demonstrated that Fis regulates the type III secretion system (T3SS) in Pseudomonas aeruginosa. In this study, we explored the role of Fis in the antibiotic resistance of P. aeruginosa and found that mutation of the fis gene increases the bacterial susceptibility to ciprofloxacin. We further demonstrated that genes related to pyocin biosynthesis are upregulated in the fis mutant. The pyocins are produced in response to genotoxic agents, including ciprofloxacin, and the release of pyocins results in lysis of the producer cell. Thus, pyocin biosynthesis genes sensitize P. aeruginosa to ciprofloxacin. We found that PrtN, the positive regulator of the pyocin biosynthesis genes, is upregulated in the fis mutant. Genetic experiments and electrophoretic mobility shift assays revealed that Fis directly binds to the promoter region of prtN and represses its expression. Therefore, our results revealed novel Fis-mediated regulation on pyocin production and bacterial resistance to ciprofloxacin in P. aeruginosa. IMPORTANCE Pseudomonas aeruginosa is an important opportunistic pathogenic bacterium that causes various acute and chronic infections in human, especially in patients with compromised immunity, cystic fibrosis (CF), and/or severe burn wounds. About 60% of cystic fibrosis patients have a chronic respiratory infection caused by P. aeruginosa. The bacterium is intrinsically highly resistant to antibiotics, which greatly increases difficulties in clinical treatment. Therefore, it is critical to understand the mechanisms and the regulatory pathways that are involved in antibiotic resistance. In this study, we elucidated a novel regulatory pathway that controls the bacterial resistance to fluoroquinolone antibiotics, which enhances our understanding of how P. aeruginosa responds to ciprofloxacin.

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