scholarly journals Acinetobacter baumannii Biofilm Formation in Human Serum and Disruption by Gallium

2016 ◽  
Vol 61 (1) ◽  
Author(s):  
Federica Runci ◽  
Carlo Bonchi ◽  
Emanuela Frangipani ◽  
Daniela Visaggio ◽  
Paolo Visca
Keyword(s):  
Human Serum ◽  
Acinetobacter Baumannii ◽  
Antibiotic Treatment ◽  
Biofilm Formation ◽  
Gallium Nitrate ◽  
Content Type ◽  
The Way

ABSTRACT Biofilm-associated infections caused by Acinetobacter baumannii are extremely recalcitrant to antibiotic treatment. We report that A. baumannii develops a mature biofilm when grown in complement-free human serum (HS). We demonstrate that 16 μM gallium nitrate (GaN) drastically reduces A. baumannii growth and biofilm formation in HS, whereas 64 μM GaN causes massive disruption of preformed A. baumannii biofilm. These findings pave the way to the repurposing of GaN as an antibiofilm agent for A. baumannii.

scholarly journals In VitroandIn VivoAntimicrobial Activities of Gallium Nitrate against Multidrug-Resistant Acinetobacter baumannii

2012 ◽  
Vol 56 (11) ◽  
pp. 5961-5970 ◽  
Author(s):  
Luísa C. S. Antunes ◽  
Francesco Imperi ◽  
Fabrizia Minandri ◽  
Paolo Visca
Keyword(s):  
Human Serum ◽  
Acinetobacter Baumannii ◽  
Galleria Mellonella ◽  
Therapeutic Potential ◽  
Survival Rates ◽  
Bloodstream Infections ◽  
Multidrug Resistant ◽  
Gallium Nitrate ◽  
Content Type ◽  
Bacterial Physiology

ABSTRACTMultidrug-resistantAcinetobacter baumanniiposes a tremendous challenge to traditional antibiotic therapy. Due to the crucial role of iron in bacterial physiology and pathogenicity, we investigated iron metabolism as a possible target for anti-A. baumanniichemotherapy using gallium as an iron mimetic. Due to chemical similarity, gallium competes with iron for binding to several redox enzymes, thereby interfering with a number of essential biological reactions. We found that Ga(NO3)3, the active component of an FDA-approved drug (Ganite), inhibits the growth of a collection of 58A. baumanniistrains in both chemically defined medium and human serum, at concentrations ranging from 2 to 80 μM and from 4 to 64 μM, respectively. Ga(NO3)3delayed the entry ofA. baumanniiinto the exponential phase and drastically reduced bacterial growth rates. Ga(NO3)3activity was strongly dependent on iron availability in the culture medium, though the mechanism of growth inhibition was independent of dysregulation of gene expression controlled by the ferric uptake regulator Fur. Ga(NO3)3also protectedGalleria mellonellalarvae from lethalA. baumanniiinfection, with survival rates of ≥75%. At therapeutic concentrations for humans (28 μM plasma levels), Ga(NO3)3inhibited the growth in human serum of 76% of the multidrug-resistantA. baumanniiisolates tested by ≥90%, raising expectations on the therapeutic potential of gallium for the treatment ofA. baumanniibloodstream infections. Ga(NO3)3also showed strong synergism with colistin, suggesting that a colistin-gallium combination holds promise as a last-resort therapy for infections caused by pan-resistantA. baumannii.

scholarly journals Interaction of Acinetobacter baumannii with Human Serum Albumin: Does the Host Determines the Outcome?

Antibiotics ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 833
Author(s):  
Camila Pimentel ◽  
Casin Le ◽  
Marisel R. Tuttobene ◽  
Tomas Subils ◽  
Krisztina M. Papp-Wallace ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Human Serum Albumin ◽  
Quorum Sensing ◽  
Serum Albumin ◽  
Human Serum ◽  
Acinetobacter Baumannii ◽  
Biofilm Formation ◽  
Model Systems ◽  
Expression Levels ◽  
Multiple Drugs

Acinetobacter baumannii has become a serious threat to human health due to its extreme antibiotic resistance, environmental persistence, and capacity to survive within the host. Two A. baumannii strains, A118 and AB5075, commonly used as model systems, and three carbapenem-resistant strains, which are becoming ever more dangerous due to the multiple drugs they can resist, were exposed to 3.5% human serum albumin (HSA) and human serum (HS) to evaluate their response with respect to antimicrobial resistance, biofilm formation, and quorum sensing, all features responsible for increasing survival and persistence in the environment and human body. Expression levels of antibiotic resistance genes were modified differently when examined in different strains. The cmlA gene was upregulated or downregulated in conditions of exposure to 3.5% HSA or HS depending on the strain. Expression levels of pbp1 and pbp3 tended to be increased by the presence of HSA and HS, but the effect was not seen in all strains. A. baumannii A118 growing in the presence of HS did not experience increased expression of these genes. Aminoglycoside-modifying enzymes were also expressed at higher or lower levels in the presence of HSA or HS. Still, the response was not uniform; in some cases, expression was enhanced, and in other cases, it was tapered. While A. baumannii AB5075 became more susceptible to rifampicin in the presence of 3.5% HSA or HS, strain A118 did not show any changes. Expression of arr2, a gene involved in resistance to rifampicin present in A. baumannii AMA16, was expressed at higher levels when HS was present in the culture medium. HSA and HS reduced biofilm formation and production of N-Acyl Homoserine Lactone, a compound intimately associated with quorum sensing. In conclusion, HSA, the main component of HS, stimulates a variety of adaptative responses in infecting A. baumannii strains.

scholarly journals Lon Protease Has Multifaceted Biological Functions inAcinetobacter baumannii

2018 ◽  
Vol 201 (2) ◽  
Author(s):  
Carly Ching ◽  
Brendan Yang ◽  
Chineme Onwubueke ◽  
David Lazinski ◽  
Andrew Camilli ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Biofilm Formation ◽  
Developmental Process ◽  
Cell Envelope ◽  
Opportunistic Pathogen ◽  
Lon Protease ◽  
Content Type ◽  
Hospital Acquired Infections ◽  
Biofilm Development ◽  
Hospital Acquired

ABSTRACTAcinetobacter baumanniiis a Gram-negative opportunistic pathogen that is known to survive harsh environmental conditions and is a leading cause of hospital-acquired infections. Specifically, multicellular communities (known as biofilms) ofA. baumanniican withstand desiccation and survive on hospital surfaces and equipment. Biofilms are bacteria embedded in a self-produced extracellular matrix composed of proteins, sugars, and/or DNA. Bacteria in a biofilm are protected from environmental stresses, including antibiotics, which provides the bacteria with selective advantage for survival. Although some gene products are known to play roles in this developmental process inA. baumannii, mechanisms and signaling remain mostly unknown. Here, we find that Lon protease inA. baumanniiaffects biofilm development and has other important physiological roles, including motility and the cell envelope. Lon proteases are found in all domains of life, participating in regulatory processes and maintaining cellular homeostasis. These data reveal the importance of Lon protease in influencing keyA. baumanniiprocesses to survive stress and to maintain viability.IMPORTANCEAcinetobacter baumanniiis an opportunistic pathogen and is a leading cause of hospital-acquired infections.A. baumanniiis difficult to eradicate and to manage, because this bacterium is known to robustly survive desiccation and to quickly gain antibiotic resistance. We sought to investigate biofilm formation inA. baumannii, since much remains unknown about biofilm formation in this bacterium. Biofilms, which are multicellular communities of bacteria, are surface attached and difficult to eliminate from hospital equipment and implanted devices. Our research identifies multifaceted physiological roles for the conserved bacterial protease Lon inA. baumannii. These roles include biofilm formation, motility, and viability. This work broadly affects and expands understanding of the biology ofA. baumannii, which will permit us to find effective ways to eliminate the bacterium.

scholarly journals Growth Retardation, Reduced Invasiveness, and Impaired Colistin-Mediated Cell Death Associated with Colistin Resistance Development in Acinetobacter baumannii

2013 ◽  
Vol 58 (2) ◽  
pp. 828-832 ◽  
Author(s):  
Spyros Pournaras ◽  
Aggeliki Poulou ◽  
Konstantina Dafopoulou ◽  
Yassine Nait Chabane ◽  
Ioulia Kristo ◽  
...  
Keyword(s):  
Cell Death ◽  
Acinetobacter Baumannii ◽  
Biofilm Formation ◽  
Bloodstream Infections ◽  
Single Amino Acid ◽  
Colistin Resistance ◽  
Resistance Development ◽  
Content Type ◽  
Alkyl Hydroperoxide ◽  
Severe Soft Tissue

ABSTRACTTwo colistin-susceptible/colistin-resistant (Cols/Colr) pairs ofAcinetobacter baumanniistrains assigned to international clone 2, which is prevalent worldwide, were sequentially recovered from two patients after prolonged colistin administration. Compared with the respective Colsisolates (Ab248 and Ab299, both having a colistin MIC of 0.5 μg/ml), both Colrisolates (Ab249 and Ab347, with colistin MICs of 128 and 32 μg/ml, respectively) significantly overexpressedpmrCABgenes, had single-amino-acid shifts in the PmrB protein, and exhibited significantly slower growth. The Colrisolate Ab347, tested by proteomic analysis in comparison with its Colscounterpart Ab299, underexpressed the proteins CsuA/B and C from thecsuoperon (which is necessary for biofilm formation). This isolate also underexpressed aconitase B and different enzymes involved in the oxidative stress response (KatE catalase, superoxide dismutase, and alkyl hydroperoxide reductase), suggesting a reduced response to reactive oxygen species (ROS) and, consequently, impaired colistin-mediated cell death through hydroxyl radical production. Colsisolates that were indistinguishable by macrorestriction analysis from Ab299 caused six sequential bloodstream infections, and isolates indistinguishable from Ab248 caused severe soft tissue infection, while Colrisolates indistinguishable from Ab347 and Ab249 were mainly colonizers. In particular, a Colsisolate identical to Ab299 was still invading the bloodstream 90 days after the colonization of this patient by Colrisolates. These observations indicate considerably lower invasiveness ofA. baumanniiclinical isolates following the development of colistin resistance.

scholarly journals Biofilm Formation Caused by Clinical Acinetobacter baumannii Isolates Is Associated with Overexpression of the AdeFGH Efflux Pump

2015 ◽  
Vol 59 (8) ◽  
pp. 4817-4825 ◽  
Author(s):  
Xinlong He ◽  
Feng Lu ◽  
Fenglai Yuan ◽  
Donglin Jiang ◽  
Peng Zhao ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Gene Transcription ◽  
Biofilm Formation ◽  
Efflux Pump ◽  
Outer Membrane Proteins ◽  
Content Type ◽  
Potential Association ◽  
Genes Encoding ◽  
Clinical Environments

ABSTRACTChronic wound infections are associated with biofilm formation, which in turn has been correlated with drug resistance. However, the mechanism by which bacteria form biofilms in clinical environments is not clearly understood. This study was designed to investigate the biofilm formation potency ofAcinetobacter baumanniiand the potential association of biofilm formation with genes encoding efflux pumps, quorum-sensing regulators, and outer membrane proteins. A total of 48 clinically isolatedA. baumanniistrains, identified by enterobacterial repetitive intergenic consensus (ERIC)-PCR as types A-II, A-III, and A-IV, were analyzed. Three representative strains, which were designatedA. baumanniiABR2, ABR11, and ABS17, were used to evaluate antimicrobial susceptibility, biofilm inducibility, and gene transcription (abaI,adeB,adeG,adeJ,carO, andompA). A significant increase in the MICs of different classes of antibiotics was observed in the biofilm cells. The formation of a biofilm was significantly induced in all the representative strains exposed to levofloxacin. The levels of gene transcription varied between bacterial genotypes, antibiotics, and antibiotic concentrations. The upregulation ofadeGcorrelated with biofilm induction. The consistent upregulation ofadeGandabaIwas detected in A-III-typeA. baumanniiin response to levofloxacin and meropenem (1/8 to 1/2× the MIC), conditions which resulted in the greatest extent of biofilm induction. This study demonstrates a potential role of the AdeFGH efflux pump in the synthesis and transport of autoinducer molecules during biofilm formation, suggesting a link between low-dose antimicrobial therapy and a high risk of biofilm infections caused byA. baumannii. This study provides useful information for the development of antibiofilm strategies.

scholarly journals Proteomic and Systematic Functional Profiling Unveils Citral Targeting Antibiotic Resistance, Antioxidant Defense, and Biofilm-Associated Two-Component Systems of Acinetobacter baumannii To Encumber Biofilm and Virulence Traits

mSystems ◽  
2020 ◽  
Vol 5 (6) ◽  
Author(s):  
Anthonymuthu Selvaraj ◽  
Alaguvel Valliammai ◽  
Pandiyan Muthuramalingam ◽  
Sivasamy Sethupathy ◽  
Ganapathy Ashwinkumar Subramenium ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Biofilm Formation ◽  
Antioxidant Defense ◽  
Time Of Flight ◽  
Differentially Expressed ◽  
Secretion Systems ◽  
Content Type ◽  
Network Analyses ◽  
Wide Range

ABSTRACT Acinetobacter baumannii has been reported as a multidrug-resistant bacterium due to biofilms and antimicrobial resistance mechanisms. Hence, novel therapeutic strategies are necessary to overcome A. baumannii infections. This study revealed that citral at 200 μg/ml attenuated A. baumannii biofilms by up to 90% without affecting viability. Furthermore, microscopic analyses and in vitro assays confirmed the antibiofilm efficacy of citral. The global effect of citral on A. baumannii was evaluated by proteomic, transcriptional, and in silico approaches. Two-dimensional (2D) gel electrophoresis and matrix-assisted laser desorption ionization–time of flight/time of flight (MALDI-TOF/TOF) analyses were used to assess the effect of citral on the A. baumannii cellular proteome. Quantitative real-time PCR (qPCR) analysis was done to validate the proteomic data and identify the differentially expressed A. baumannii genes. Protein-protein interactions, gene enrichment, and comparative gene network analyses were performed to explore the interactions and functional attributes of differentially expressed proteins of A. baumannii. Global omics-based analyses revealed that citral targeted various mechanisms such as biofilm formation, antibiotic resistance, antioxidant defense, iron acquisition, and type II and type IV secretion systems. The results of antioxidant analyses and antibiotic sensitivity, blood survival, lipase, and hemolysis assays validated the proteomic results. Cytotoxicity analysis showed a nontoxic effect of citral on peripheral blood mononuclear cells (PBMCs). Overall, the current study unveiled that citral has multitarget efficacy to inhibit the biofilm formation and virulence of A. baumannii. IMPORTANCE Acinetobacter baumannii is a nosocomial-infection-causing bacterium and also possesses multidrug resistance to a wide range of conventional antibiotics. The biofilm-forming ability of A. baumannii plays a major role in its resistance and persistence. There is an alarming need for novel treatment strategies to control A. baumannii biofilm-associated issues. The present study demonstrated the strong antibiofilm and antivirulence efficacy of citral against A. baumannii. In addition, proteomic analysis revealed the multitarget potential of citral against A. baumannii. Furthermore, citral treatment enhances the susceptibility of A. baumannii to the host innate immune system and reactive oxygen species (ROS). Cytotoxicity analysis revealed the nonfatal effect of citral on human PBMCs. Therefore, citral could be the safest therapeutic compound and can be taken for further clinical evaluation for the treatment of biofilm-associated infections by A. baumannii.

scholarly journals Impact of a Cross-Kingdom Signaling Molecule of Candida albicans on Acinetobacter baumannii Physiology

2015 ◽  
Vol 60 (1) ◽  
pp. 161-167 ◽  
Author(s):  
Xenia Kostoulias ◽  
Gerald L. Murray ◽  
Gustavo M. Cerqueira ◽  
Jason B. Kong ◽  
Farkad Bantun ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Cell Membrane ◽  
Acinetobacter Baumannii ◽  
Biofilm Formation ◽  
Defense Mechanism ◽  
Membrane Integrity ◽  
Efflux Pumps ◽  
Signaling Molecule ◽  
Content Type ◽  
Antagonistic Interactions

ABSTRACTMultidrug-resistant (MDR)Acinetobacter baumanniiis an opportunistic human pathogen that has become highly problematic in the clinical environment. Novel therapies are desperately required. To assist in identifying new therapeutic targets, the antagonistic interactions betweenA. baumanniiand the most common human fungal pathogen,Candida albicans, were studied. We have observed that theC. albicansquorum-sensing molecule, farnesol, has cross-kingdom interactions, affecting the viability ofA. baumannii. To gain an understanding of its mechanism, the transcriptional profile ofA. baumanniiexposed to farnesol was examined. Farnesol caused dysregulation of a large number of genes involved in cell membrane biogenesis, multidrug efflux pumps (AcrAB-like and AdeIJK-like), andA. baumanniivirulence traits such as biofilm formation (csuA,csuB, andompA) and motility (pilZandpilH). We also observed a strong induction in genes involved in cell division (minD,minE,ftsK,ftsB, andftsL). These transcriptional data were supported by functional assays showing that farnesol disruptsA. baumanniicell membrane integrity, alters cell morphology, and impairs virulence characteristics such as biofilm formation and twitching motility. Moreover, we showed thatA. baumanniiuses efflux pumps as a defense mechanism against this eukaryotic signaling molecule. Owing to its effects on membrane integrity, farnesol was tested to see if it potentiated the activity of the membrane-acting polymyxin antibiotic colistin. When coadministered, farnesol increased sensitivity to colistin for otherwise resistant strains. These data provide mechanistic understanding of the antagonistic interactions between diverse pathogens and may provide important insights into novel therapeutic strategies.

scholarly journals Defining Gene-Phenotype Relationships in Acinetobacter baumannii through One-Step Chromosomal Gene Inactivation

mBio ◽  
2014 ◽  
Vol 5 (4) ◽  
Author(s):  
Ashley T. Tucker ◽  
Emily M. Nowicki ◽  
Joseph M. Boll ◽  
Gregory A. Knauf ◽  
Nora C. Burdis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Genome Editing ◽  
Biofilm Formation ◽  
Content Type ◽  
Stress Protection ◽  
Biocide Resistance ◽  
Hospital Acquired ◽  
Oxidative Stress Protection

ABSTRACTRates of infection with hospital-acquiredAcinetobacter baumanniihave exploded over the past decade due to our inability to limit persistence and effectively treat disease.A. baumanniiquickly acquires antibiotic resistance, and its genome encodes mechanisms to tolerate biocides and desiccation, which enhance its persistence in hospital settings. With depleted antibiotic options, new methods to treatA. baumanniiinfections are desperately needed. A comprehensive understanding detailingA. baumanniicellular factors that contribute to its resiliency at genetic and mechanistic levels is vital to the development of new treatment options. Tools to rapidly dissect theA. baumanniigenome will facilitate this goal by quickly advancing our understanding ofA. baumanniigene-phenotype relationships. We describe here a recombination-mediated genetic engineering (recombineering) system for targeted genome editing ofA. baumannii. We have demonstrated that this system can perform directed mutagenesis on wide-ranging genes and operons and is functional in various strains ofA. baumannii, indicating its broad application. We utilized this system to investigate key gene-phenotype relationships inA. baumanniibiology important to infection and persistence in hospitals, including oxidative stress protection, biocide resistance mechanisms, and biofilm formation. In addition, we have demonstrated that both the formation and movement of type IV pili play an important role inA. baumanniibiofilm.IMPORTANCEAcinetobacter baumanniiis the causative agent of hospital-acquired infections, including pneumonia and serious blood and wound infections.A. baumanniiis an emerging pathogen and has become a threat to public health because it quickly develops antibiotic resistance, making treatment difficult or impossible. While the threat ofA. baumanniiis well recognized, our understanding of even its most basic biology lags behind. Analysis ofA. baumanniicellular functions to identify potential targets for drug development has stalled due in part to laborious genetic techniques. Here we have pioneered a novel recombineering system that facilitates efficient genome editing inA. baumanniiby single PCR products. This technology allows for rapid genome editing to quickly ascertain gene-phenotype relationships. To demonstrate the power of recombineering in dissectingA. baumanniibiology, we use this system to establish key gene-phenotype relationships important to infection and persistence in hospitals, including oxidative stress protection, biocide resistance, and biofilm formation.

scholarly journals Molecular Analysis of the Acinetobacter baumannii Biofilm-Associated Protein

2013 ◽  
Vol 79 (21) ◽  
pp. 6535-6543 ◽  
Author(s):  
H. M. Sharon Goh ◽  
Scott A. Beatson ◽  
Makrina Totsika ◽  
Danilo G. Moriel ◽  
Minh-Duy Phan ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Biofilm Formation ◽  
Multidrug Resistant ◽  
Hospital Environment ◽  
Biofilm Growth ◽  
Content Type ◽  
Amino Acid Region ◽  
Carbapenem Resistant ◽  
C Terminus ◽  
And Function

ABSTRACTAcinetobacter baumanniiis a multidrug-resistant pathogen associated with hospital outbreaks of infection across the globe, particularly in the intensive care unit. The ability ofA. baumanniito survive in the hospital environment for long periods is linked to antibiotic resistance and its capacity to form biofilms. Here we studied the prevalence, expression, and function of theA. baumanniibiofilm-associated protein (Bap) in 24 carbapenem-resistantA. baumanniiST92 strains isolated from a single institution over a 10-year period. Thebapgene was highly prevalent, with 22/24 strains being positive forbapby PCR. Partial sequencing ofbapwas performed on the index case strain MS1968 and revealed it to be a large and highly repetitive gene approximately 16 kb in size. Phylogenetic analysis employing a 1,948-amino-acid region corresponding to the C terminus of Bap showed that BapMS1968clusters with Bap sequences from clonal complex 2 (CC2) strains ACICU, TCDC-AB0715, and 1656-2 and is distinct from Bap in CC1 strains. By using overlapping PCR, thebapMS1968gene was cloned, and its expression in a recombinantEscherichia colistrain resulted in increased biofilm formation. A Bap-specific antibody was generated, and Western blot analysis showed that the majority ofA. baumanniistrains expressed an ∼200-kDa Bap protein. Further analysis of three Bap-positiveA. baumanniistrains demonstrated that Bap is expressed at the cell surface and is associated with biofilm formation. Finally, biofilm formation by these Bap-positive strains could be inhibited by affinity-purified Bap antibodies, demonstrating the direct contribution of Bap to biofilm growth byA. baumanniiclinical isolates.

scholarly journals Pyoverdine and Proteases Affect the Response of Pseudomonas aeruginosa to Gallium in Human Serum

2015 ◽  
Vol 59 (9) ◽  
pp. 5641-5646 ◽  
Author(s):  
Carlo Bonchi ◽  
Emanuela Frangipani ◽  
Francesco Imperi ◽  
Paolo Visca
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Human Serum ◽  
Bloodstream Infections ◽  
Proteinase K ◽  
Gallium Nitrate ◽  
Iron Availability ◽  
Content Type ◽  
Iron Restriction ◽  
Casamino Acids

ABSTRACTGallium is an iron mimetic which has recently been repurposed as an antibacterial agent due to its capability to disrupt bacterial iron metabolism. In this study, the antibacterial activity of gallium nitrate [Ga(NO3)3] was investigated in complement-free human serum (HS) on 55Pseudomonas aeruginosaclinical isolates from cystic fibrosis and non-cystic fibrosis patients. The susceptibility ofP. aeruginosato Ga(NO3)3in HS was dependent on the bacterial ability to acquire iron from serum binding proteins (i.e., transferrin). The extent of serum protein degradation correlated well withP. aeruginosagrowth in HS, while pyoverdine production did not. However, pyoverdine-deficientP. aeruginosastrains were unable to grow in HS and overcome iron restriction, albeit capable of releasing proteases. Predigestion of HS with proteinase K promoted the growth of all strains, irrespective of their ability to produce proteases and/or pyoverdine. The MICs of Ga(NO3)3were higher in HS than in an iron-poor Casamino Acids medium, where proteolysis does not affect iron availability. Coherently, strains displaying high proteolytic activity were less susceptible to Ga(NO3)3in HS. Our data support a model in which both pyoverdine and proteases affect the response ofP. aeruginosato Ga(NO3)3in HS. The relatively high Ga(NO3)3concentration required to inhibit the growth of highly proteolyticP. aeruginosaisolates in HS poses a limitation to the potential of Ga(NO3)3in the treatment ofP. aeruginosabloodstream infections.

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