TypA is involved in virulence, antimicrobial resistance and biofilm formation in Pseudomonas aeruginosa

Neidig, Anke; Yeung, Amy; Rosay, Thibaut; Tettmann, Beatrix; Strempel, Nikola; Rueger, Martina; Lesouhaitier, Olivier; Overhage, J. Marc

doi:10.1186/1471-2180-13-77

Cited by 73 publications

(75 citation statements)

References 53 publications

(79 reference statements)

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“…aeruginosa is a leading cause of health-care associated infections [9] and is extremely difficult to treat due to its high intrinsic and adaptive antibiotic resistance [10]. Despite the discovery of ESBL, Amp C β-lactamase and MBL at least a decade ago, there remains a low level of awareness of their importance and many clinical laboratories do not undergo routine detection of ESBL& Amp C β-lactamase.…”

Section: Discussionmentioning

confidence: 99%

Lab Based Surveillance of Multidrug Resistant Pseudomonas aeruginosa in Cairo University Hospitals, Egypt

Zafer¹

2015

JMEN

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Multidrug resistance is increasingly recorded among P. aeruginosa causing health care associated infections (HAI) due to the selective pressure by over-usage of antibiotics. The primary aim of the study was to perform a laboratory based surveillance to investigate the prevalence of β-lactamase and AmpC production and multi-drug resistance among clinical isolates of P. aeruginosa causing health care associated infections in Kasr Al Aini School of Medicine and National Cancer Institute, Cairo University, Egypt. β-lactamase and AmpC production was tested by the double disc test. Multidrug-resistant P. aeruginosa (MDRPA) were defined as demonstrating resistance to carbapenems, all anti-pseudomonal cephalosporins, amino glycosides and fluoroquinolones. In a six months period, out of 12,524 clinical samples, 2593 (20.7%) P. aeruginosa isolates were identified. Out of these isolates, 1138 (43.9%) were ceftazidime resistant, 138 (5.3%) were ESBL producers, and 661 (25.5%) isolates were confirmed positive for inducible AmpC beta-lactamase. The proportion of multidrug-resistant P. aeruginosa was 12.3%. In conclusion, high prevalence of AmpC indicates the necessity of performing routine tests to detect AmpC in ceftazidime resistant P. aeruginosa isolates. Lab based surveillance is important to identify the prevalence of MDRPA in order to guide empirical antibiotic therapy and prevent the spread of resistant strains.

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Section: Discussionmentioning

confidence: 99%

Lab Based Surveillance of Multidrug Resistant Pseudomonas aeruginosa in Cairo University Hospitals, Egypt

Zafer¹

2015

JMEN

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“…BipA (BPI-inducible protein A) gene is highly conserved among bacterial and chloroplast genomes (4) and has been implicated in regulating a variety of cellular processes including bacterial virulence, symbiosis, various stress responses, resistance to host defenses, swarming motility, biofilm, and capsule formation (8)(9)(10). As is the case with EF4, BipA is not required under optimal growth conditions but becomes an essential factor for bacterial survival at low temperature, nutrient depletion, and various other stress conditions (1,9).…”

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confidence: 99%

Structure of BipA in GTP form bound to the ratcheted ribosome

Kumar

Chen

Ero

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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BPI-inducible protein A (BipA) is a member of the family of ribosome-dependent translational GTPase (trGTPase) factors along with elongation factors G and 4 (EF-G and EF4). Despite being highly conserved in bacteria and playing a critical role in coordinating cellular responses to environmental changes, its structures (isolated and ribosome bound) remain elusive. Here, we present the crystal structures of apo form and GTP analog, GDP, and guanosine-3′,5′-bisdiphosphate (ppGpp)-bound BipA. In addition to having a distinctive domain arrangement, the C-terminal domain of BipA has a unique fold. Furthermore, we report the cryo-electron microscopy structure of BipA bound to the ribosome in its active GTP form and elucidate the unique structural attributes of BipA interactions with the ribosome and A-site tRNA in the light of its possible function in regulating translation.

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“…Adhesion assays were performed as previously described with minor modifications (22). Following PAO1 activation, the control and hyperoside groups were cultured in a 96-well microtiter plate and incubated for 4 h at 37˚C.…”

Section: Microscopy Analysismentioning

confidence: 99%

Hyperoside inhibits biofilm formation of Pseudomonas aeruginosa

Sun

Feng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Pseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infection and is readily able to form biofilms. Due to its high antibiotic resistance, traditional antibacterial treatments exert a limited effect on P. aeruginosa biofilm infections. It has been indicated that hyperoside inhibits P. aeruginosa PAO1 (PAO1) biofilm formation without affecting growth. Therefore, the current study examined the biofilm formation and quorum sensing (QS) system of PAO1 in the presence of hyperoside.Confocal laser scanning microscopy analysis demonstrated that hyperoside significantly inhibited biofilm formation. It was also observed that hyperoside inhibited twitching motility in addition to adhesion. Data from reverse transcription-quantitative polymerase chain reaction indicated that hyperoside inhibited the expression of lasR, lasI, rhlR and rhlI genes. These results suggest that the QS-inhibiting effect of hyperoside may lead to a reduction in biofilm formation. However, the precise mechanism of hyperoside on P. aeruginosa pathogenicity remains unclear and requires elucidation in additional studies. IntroductionPseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infections (1). Due to increasing multidrug resistance, P. aeruginosa infection is an increasingly common cause of mortality and morbidity (2). The mechanisms of antibiotic resistance in P. aeruginosa include the expression of multiple antibiotic modifying enzymes, antibiotic efflux pumps and acquisition of chromosomally or plasmid encoded antibiotic resistance genes. Additionally, chromosomal mutations and lower membrane permeability for the antibiotics also contribute to antibiotic resistance (3).P. aeruginosa is a biofilm-forming pathogen and is difficult to eradicate due to its high antibiotic resistance and the ability of the biofilm to evade the immune system (4-7). Quorum sensing (QS) is a system of stimuli and response correlated to population density. P. aeruginosa uses the QS system to coordinate gene expression according to the density of its local population. Thus, it can coordinate certain behaviors such as biofilm formation, virulence and antibiotic resistance. QS inhibitors (QSIs) are the most well reported alternative therapeutics that can be used to overcome the problem of increasing antibiotic resistance in P. aeruginosa. QSIs target the virulence of the organism and therefore are also termed antipathogenic drugs. The virulence of P. aeruginosa depends on its cell-to-cell communication system, or QS system that uses diffusible signaling molecules that accumulate with increasing cell density and allows P. aeruginosa to trigger coordinated responses and achieve outcomes that would otherwise remain impossible to achieve by individual bacterium (8). Previous studies have demonstrated that traditional treatments for bacteria exert some effect on biofilm infections (9,10). Therefore, the effects of constituents from marine organisms, traditional Chinese herbs and plants (11-13) on biofilm infe...

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TypA is involved in virulence, antimicrobial resistance and biofilm formation in Pseudomonas aeruginosa

Cited by 73 publications

References 53 publications

Lab Based Surveillance of Multidrug Resistant Pseudomonas aeruginosa in Cairo University Hospitals, Egypt

Lab Based Surveillance of Multidrug Resistant Pseudomonas aeruginosa in Cairo University Hospitals, Egypt

Structure of BipA in GTP form bound to the ratcheted ribosome

Hyperoside inhibits biofilm formation of Pseudomonas aeruginosa

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