Pathogenic Escherichia coli change the adhesion between neutrophils and endotheliocytes in the experimental bacteremia model

Authors:

Svetlana N Pleskova1,2,*, Nikolay A Bezrukov1, Sergey Z Bobyk1, Ekaterina N Gorshkova1 and Dimitri V Novikov3

doi: 10.15698/mic2024.07.830
Volume 11, pp. 254 to 264, published 22/07/2024.

Affiliations:

1 Research Laboratory of Scanning Probe Microscopy, Lobachevsky State University of Nizhny Novgorod, Nizhny Novgorod, Russia. 2 Nanotechnology and Biotechnology” Department, Nizhny Novgorod State Technical University named after Alekseev R.E., Nizhny Novgorod, Russia. 3 Nizhny Novgorod Research Institute of Epidemiology and microbiology named after Blokhina I.N., Nizhny Novgorod, Russia.

Keywords: 

neutrophils, endothelial cells, Escherichia coli, adhesion force, adhesion work, FS spectroscopy, apoptosis, stiffness of membrane-cytoskeleton complex.

Corresponding Author(s):

Conflict of interest statement:

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Please cite this article as:

Svetlana N Pleskova, Nikolay A Bezrukov, Sergey Z Bobyk, Ekaterina N Gorshkova, Dmitri V Novikov (2024). Pathogenic Escherichia coli change the adhesion between neutrophils and endotheliocytes in the experimental bacteremia model. Microbial Cell 11: 254-264. doi: 10.15698/mic2024.07.830

© 2024 Pleskova et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

Septicemia caused by gram-negative bacteria is characterized by high death rate due to the endotoxin release. Since the septicemia depends not only on biochemical aspects of interactions in the system bloodstream, the study of mechanical interactions is also important. Using a model of experimental septicemia caused by E. coli, a hyperproduction of integrins CD11a and CD11b by neutrophils was shown, but this did not lead to the establishment of strong  adhesion contacts between endothelial cells and neutrophils. On the contrary, adhesion force and work, as assessed by FS spectroscopy, were statistically significantly reduced in the presence of bacteria. It has also been shown that  exposure to the pathogenic strain E. coli 321 increases the stiffness of the membrane-cytoskeleton complex of endothelial cells and bacteria significantly change their morphology on long-term observation. At the same time, we observed the death of neutrophils by apoptosis. Thus, it was shown that besides lipopolysaccharide release there are other pathogenic factors of E. coli: decrease in the interaction between neutrophil and endothelial cell caused by an increase of the endothelial cell rigidity and apoptotic death of neutrophils probably as a result of adhesins and exotoxin effects. Obtained results should be taken in mind during the therapy of septicemia.