Effect of sub-inhibitory antibacterial stress on bacterial surface properties and biofilm formation

2013 ◽  
Vol 111 ◽  
pp. 747-754 ◽  
Author(s):  
Amit Kumar ◽  
Yen-Peng Ting
2015 ◽  
Vol 127 ◽  
pp. 182-191 ◽  
Author(s):  
Rohit Ruhal ◽  
Henrik Antti ◽  
Olena Rzhepishevska ◽  
Nicolas Boulanger ◽  
David R. Barbero ◽  
...  

2013 ◽  
Vol 62 (5) ◽  
pp. 754-760 ◽  
Author(s):  
D. L. R. Gomes ◽  
R. S. Peixoto ◽  
E. A. B. Barbosa ◽  
F. Napoleão ◽  
P. S. Sabbadini ◽  
...  

Subinhibitory concentrations (subMICs) of antibiotics may alter bacterial surface properties and change microbial physiology. This study aimed to investigate the effect of a subMIC (⅛ MIC) of penicillin (PEN) and erythromycin (ERY) on bacterial morphology, haemagglutinating activity, cell-surface hydrophobicity (CSH) and biofilm formation on glass and polystyrene surfaces, as well as the distribution of cell-surface acidic anionic residues of Corynebacterium diphtheriae strains (HC01 tox − strain; CDC-E8392 and 241 tox + strains). All micro-organisms tested were susceptible to PEN and ERY. Growth in the presence of PEN induced bacterial filamentation, whereas subMIC of ERY caused cell-size reduction of strains 241 and CDC-E8392. Adherence to human erythrocytes was reduced after growth in the presence of ERY, while CSH was increased by a subMIC of both antibiotics in bacterial adherence to n-hexadecane assays. Conversely, antibiotic inhibition of biofilm formation was not observed. All strains enhanced biofilm formation on glass after treatment with ERY, while only strain 241 increased glass adherence after cultivation in the presence of PEN. Biofilm production on polystyrene surfaces was improved by ⅛ MIC of ERY. After growth in the presence of both antimicrobial agents, strains 241 and CDC-E8392 exhibited anionic surface charges with focal distribution. In conclusion, subMICs of PEN and ERY modified bacterial surface properties and enhanced not only biofilm formation but also cell-surface hydrophobicity. Antibiotic-induced biofilm formation may contribute to the inconsistent success of antimicrobial therapy for C. diphtheriae infections.


2007 ◽  
Vol 26 (5) ◽  
pp. 613-622 ◽  
Author(s):  
Masahiro ONO ◽  
Toru NIKAIDO ◽  
Masaomi IKEDA ◽  
Susumu IMAI ◽  
Nobuhiro HANADA ◽  
...  

Biomaterials ◽  
2010 ◽  
Vol 31 (36) ◽  
pp. 9462-9472 ◽  
Author(s):  
Bidhari Pidhatika ◽  
Jens Möller ◽  
Edmondo M. Benetti ◽  
Rupert Konradi ◽  
Ekaterina Rakhmatullina ◽  
...  

2006 ◽  
Vol 112 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Mai Huong Ly ◽  
Murielle Naïtali-Bouchez ◽  
Thierry Meylheuc ◽  
Marie-Noëlle Bellon-Fontaine ◽  
Thanh Mai Le ◽  
...  

2010 ◽  
Vol 78 (10) ◽  
pp. 4268-4275 ◽  
Author(s):  
Oonagh Shannon ◽  
Matthias Mörgelin ◽  
Magnus Rasmussen

ABSTRACT The Gram-positive bacterium Aerococcus urinae can cause infectious endocarditis (IE) in older persons. Biofilm formation and platelet aggregation are believed to contribute to bacterial virulence in IE. Five A. urinae isolates from human blood were shown to form biofilms in vitro, and biofilm formation was enhanced by the presence of human plasma. Four of the A. urinae isolates caused platelet aggregation in platelet-rich plasma from healthy donors. The Au3 isolate, which induced platelet aggregation in all donors, also activated platelets, as determined by flow cytometry. Platelet aggregation was dependent on bacterial protein structures and on platelet activation since it was sensitive to both trypsin and prostaglandin E1. Plasma proteins at the bacterial surface were needed for platelet aggregation; and roles of the complement system, fibrinogen, and immunoglobulin G were demonstrated. Complement-depleted serum was unable to support platelet aggregation by Au3 and complement blockade using compstatin-inhibited platelet activation. Platelet activation by Au3 was inhibited by blocking of the platelet fibrinogen receptor, and this isolate was also shown to bind to radiolabeled fibrinogen. Removal of IgG from platelet-rich plasma by a specific protease inhibited the platelet aggregation induced by A. urinae, and blockade of the platelet FcRγIIa hindered platelet activation induced by Au3. Convalescent-phase serum from a patient with A. urinae IE transferred the ability of the bacterium to aggregate platelets in an otherwise nonresponsive donor. Our results show that A. urinae exhibits virulence strategies of importance for IE.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Seon Hee Woo ◽  
Sang Moog Lee ◽  
Ki Cheol Park ◽  
Gyeong Nam Park ◽  
Byeolnimhee Cho ◽  
...  

Respiratory infections ofPseudomonas aeruginosaare a major cause of mortality and morbidity for hospitalized patients. Fine particulate matter (FPM) is known to have interactions with some bacterial infection in the respiratory system. In this report, we investigate the effect of different concentration of FPM onP. aeruginosaattachment and biofilm formation usingin vitrocell culture systems.P. aeruginosawere cultured to form mature biofilms on hydroxyapatite-coated peg and the number of bacteria in the biofilms was enumerated. Morphology of biofilm was imaged with scanning electron microscopy and confocal laser scanning microscopy. Bacterial affinity change to the cell membrane was evaluated with attached colony counting and fluorescence microscopy images. Alteration of bacterial surface hydrophobicity and S100A4 protein concentration were explored as mechanisms ofP. aeruginosaadhesion to human cells. There were a concentration-dependent increase of thickness and surface roughness of biofilm mass.P. aeruginosaadherence to respiratory epithelial cells was increased after FPM treatment. Bacterial surface hydrophobicity and S1000A4 protein concentration were increased with proportionally the dose of FPM in media. FPM in the airway could enhance both the adhesion ofP. aeruginosato epithelial cells and biofilm formation. Bacterial surface hydrophobicity and human cell plasma membrane injury are associated with binding ofP. aeruginosaon airway epithelial cells and biofilm formation.


2018 ◽  
Vol 31 (10) ◽  
pp. 1075-1082 ◽  
Author(s):  
Fernando Sorroche ◽  
Pablo Bogino ◽  
Daniela M. Russo ◽  
Angeles Zorreguieta ◽  
Fiorela Nievas ◽  
...  

Bacterial surface molecules are crucial for the establishment of a successful rhizobia-legume symbiosis, and, in most bacteria, are also critical for adherence properties, surface colonization, and as a barrier for defense. Rhizobial mutants defective in the production of exopolysaccharides (EPSs), lipopolysaccharides (LPSs), or capsular polysaccharides are usually affected in symbiosis with their plant hosts. In the present study, we evaluated the role of the combined effects of LPS and EPS II in cell-to-cell and cell-to-surface interactions in Sinorhizobium meliloti by studying planktonic cell autoaggregation, biofilm formation, and symbiosis with the host plant Medicago sativa. The lpsB mutant, which has a defective core portion of LPS, exhibited a reduction in biofilm formation on abiotic surfaces as well as altered biofilm architecture compared with the wild-type Rm8530 strain. Atomic force microscopy and confocal laser microscopy revealed an increase in polar cell-to-cell interactions in the lpsB mutant, which might account for the biofilm deficiency. However, a certain level of biofilm development was observed in the lpsB strain compared with the EPS II-defective mutant strains. Autoaggregation experiments carried out with LPS and EPS mutant strains showed that both polysaccharides have an impact on the cell-to-cell adhesive interactions of planktonic bacteria. Although the lpsB mutation and the loss of EPS II production strongly stimulated early attachment to alfalfa roots, the number of nodules induced in M. sativa was not increased. Taken together, this work demonstrates that S. meliloti interactions with biotic and abiotic surfaces depend on the interplay between LPS and EPS II.


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