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在实验性菌血症模型中,病原体改变了中性粒细胞与内皮细胞之间的黏附。

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

作者信息

Pleskova Svetlana N, Bezrukov Nikolay A, Bobyk Sergey Z, Gorshkova Ekaterina N, Novikov Dmitri V

机构信息

Research Laboratory of Scanning Probe Microscopy, Lobachevsky State University of Nizhny Novgorod Nizhny Novgorod Russia.

"Nanotechnology and Biotechnology" Department, Nizhny Novgorod State Technical University named after Alekseev R.E. Nizhny Novgorod Russia.

出版信息

Microb Cell. 2024 Jul 22;11:254-264. doi: 10.15698/mic2024.07.830. eCollection 2024.

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 , 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 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 : 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.

摘要

革兰氏阴性菌引起的败血症以内毒素释放导致的高死亡率为特征。由于败血症不仅取决于血液循环系统中相互作用的生化方面,机械相互作用的研究也很重要。使用由[具体病因未提及]引起的实验性败血症模型,显示中性粒细胞整合素CD11a和CD11b过度产生,但这并未导致内皮细胞与中性粒细胞之间形成强粘附接触。相反,通过FS光谱评估的粘附力和功在有细菌存在时在统计学上显著降低。还表明,暴露于致病菌株321会增加内皮细胞膜 - 细胞骨架复合物的硬度,并且长期观察发现细菌会显著改变其形态。同时,我们观察到中性粒细胞通过凋亡死亡。因此,研究表明,除了脂多糖释放外,[具体病因未提及]还有其他致病因素:内皮细胞硬度增加导致中性粒细胞与内皮细胞之间的相互作用减少,以及中性粒细胞的凋亡死亡可能是由于粘附素和外毒素的作用。在败血症治疗过程中应考虑到所获得的结果。

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