scholarly journals Glycerol and ethylene glycol: members of a new class of repellents of Escherichia coli chemotaxis.

1983 ◽  
Vol 154 (1) ◽  
pp. 104-112 ◽  
Author(s):  
K Oosawa ◽  
Y Imae
2021 ◽  
Author(s):  
Zhengzhong Tan ◽  
Ziyuan Song ◽  
Tianrui Xue ◽  
Lining Zheng ◽  
Lei Jiang ◽  
...  

With PEG-like properties, such as hydrophilicity and stealth effect against protein absorption, oligo(ethylene glycol) (OEG)-functionalized polypeptides have emerged as a new class of biomaterials alternative to PEG with polypeptide-like properties....


1996 ◽  
Vol 29 (11) ◽  
pp. 3831-3838 ◽  
Author(s):  
Craig J. Hawker ◽  
Fengkui Chu ◽  
Peter J. Pomery ◽  
David J. T. Hill

Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 263
Author(s):  
Fabian Schröer ◽  
Tanja J. Paul ◽  
Dimitri Wilms ◽  
Torben H. Saatkamp ◽  
Nicholas Jäck ◽  
...  

The synthesis of carbohydrate-functionalized biocompatible poly(oligo(ethylene glycol) methacrylate microgels and the analysis of the specific binding to concanavalin A (ConA) and Escherichia coli (E. coli) is shown. By using different crosslinkers, the microgels’ size, density and elastic modulus were varied. Given similar mannose (Man) functionalization degrees, the softer microgels show increased ConA uptake, possibly due to increased ConA diffusion in the less dense microgel network. Furthermore, although the microgels did not form clusters with E. coli in solution, surfaces coated with mannose-functionalized microgels are shown to bind the bacteria whereas galactose (Gal) and unfunctionalized microgels show no binding. While ConA binding depends on the overall microgels’ density and Man functionalization degree, E. coli binding to microgels’ surfaces appears to be largely unresponsive to changes of these parameters, indicating a rather promiscuous surface recognition and sufficiently strong anchoring to few surface-exposed Man units. Overall, these results indicate that carbohydrate-functionalized biocompatible oligo(ethylene glycol)-based microgels are able to immobilize carbohydrate binding pathogens specifically and that the binding of free lectins can be controlled by the network density.


2013 ◽  
Vol 62 (6) ◽  
pp. 896-905 ◽  
Author(s):  
David T. Bolick ◽  
James K. Roche ◽  
Raquel Hontecillas ◽  
Josep Bassaganya-Riera ◽  
James P. Nataro ◽  
...  

Enteroaggregative Escherichia coli (EAEC) is increasingly recognized as a common cause of diarrhoea in healthy, malnourished and immune-deficient adults and children. There is no reproducible non-neonatal animal model for longitudinal studies of disease mechanism or therapy. Using two strains of human-derived EAEC to challenge weaned C57BL/6 mice, we explored an in vivo model of EAEC infection in mice, in which disease was monitored quantitatively as the growth rate, stool shedding and tissue burden of organisms; nutritional status was varied, and a new class of therapeutics was assessed. A single oral challenge of EAEC strain 042 resulted in significant growth shortfalls (5–8 % of body weight in 12 days), persistent shedding of micro-organisms in stools [>103.2 c.f.u. (10 mg stool)−1 for at least 14 days] and intestinal tissue burden [~103 c.f.u. (10 mg tissue)−1 detectable up to 14 days post-challenge]. Moderate malnourishment of mice using a ‘regional basic diet’ containing 7 % protein and reduced fat and micronutrients heightened all parameters of infection. Nitazoxanide in subMIC doses, administered for 3 days at the time of EAEC challenge, lessened growth shortfalls (by >10 % of body weight), stool shedding [by 2–3 logs (10 mg stool)−1] and tissue burden of organisms (by >75 % in the jejunum and colon). Thus, weaned C57BL/6 mice challenged with EAEC is a convenient, readily inducible model of EAEC infection with three highly quantifiable outcomes in which disease severity is dependent on the nutritional status of the host, and which is modifiable in the presence of inhibitors of pyruvate ferredoxin oxidoreductase such as nitazoxanide.


2015 ◽  
Vol 113 (2) ◽  
pp. 376-383 ◽  
Author(s):  
Brian Pereira ◽  
Haoran Zhang ◽  
Marjan De Mey ◽  
Chin Giaw Lim ◽  
Zheng-Jun Li ◽  
...  

2000 ◽  
Vol 68 (4) ◽  
pp. 2148-2155 ◽  
Author(s):  
Jan-Michael A. Klapproth ◽  
Isabel C. A. Scaletsky ◽  
Barry P. McNamara ◽  
Li-Ching Lai ◽  
Carol Malstrom ◽  
...  

ABSTRACT The mechanisms by which bacteria resist cell-mediated immune responses to cause chronic infections are largely unknown. We report the identification of a large gene present in enteropathogenic strains of Escherichia coli (EPEC) that encodes a toxin that specifically inhibits lymphocyte proliferation and interleukin-2 (IL-2), IL-4, and gamma interferon production in response to a variety of stimuli. Lymphostatin, the product of this gene, is predicted to be 366 kDa and shares significant homology with the catalytic domains of the large clostridial cytotoxins. A mutant EPEC strain that has a disruption in this gene lacks the ability to inhibit lymphokine production and lymphocyte proliferation. Enterohemorrhagic E. coli strains of serotype O157:H7 possess a similar gene located on a large plasmid. Loss of the plasmid is associated with loss of the ability to inhibit IL-2 expression while transfer of the plasmid to a nonpathogenic strain of E. coli is associated with gain of this activity. Among 89 strains of E. coli and related bacteria tested, lifA sequences were detected exclusively in strains capable of attaching and effacing activity. Lymphostatin represents a new class of large bacterial toxins that blocks lymphocyte activation.


2017 ◽  
Vol 97 ◽  
pp. 11-20 ◽  
Author(s):  
Rhudith B. Cabulong ◽  
Kris Niño G. Valdehuesa ◽  
Kristine Rose M. Ramos ◽  
Grace M. Nisola ◽  
Won-Keun Lee ◽  
...  

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