Speed-dependent bacterial surface swimming.

Solid surfaces submerged in liquid in natural environments alter bacterial swimming behavior and serve as platforms for bacteria to form biofilms. In the initial stage of biofilm formation, bacteria detect surfaces and increase the intracellular level of the second messenger c-di-GMP, leading to a reduction in swimming speed. The impact of this speed reduction on bacterial surface swimming remains unclear. In this study, we utilized advanced microscopy techniques to examine the effect of swimming speed on bacterial surface swimming behavior. We found that a decrease in swimming speed reduces the cell-surface distance and prolongs the surface trapping time. Both these effects would enhance bacterial surface sensing and increase the likelihood of cells adhering to the surface, thereby promoting biofilm formation. We also examined the surface-escaping behavior of wild-type Escherichia coli and Pseudomonas aeruginosa, noting distinct surface-escaping mechanisms between the two bacterial species. IMPORTANCE: In the early phase of biofilm formation, bacteria identify surfaces and increase the intracellular level of the second messenger c-di-GMP, resulting in a decrease in swimming speed. Here, we utilized advanced microscopy techniques to investigate the impact of swimming speed on bacterial surface swimming, focusing on Escherichia coli and Pseudomonas aeruginosa. We found that an increase in swimming speed led to an increase in the radius of curvature and a decrease in surface detention time. These effects were explained through hydrodynamic modeling as a result of an increase in the cell-surface distance with increasing swimming speed. We also observed distinct surface-escaping mechanisms between the two bacterial species. Our study suggests that a decrease in swimming speed could enhance the likelihood of cells adhering to the surface, promoting biofilm formation. This sheds light on the role of reduced swimming speed in the transition from motile to sedentary bacterial lifestyles.

Bacterial surface swimming states revealed by TIRF microscopy.

Motility near solid surfaces plays a key role in the life cycle of bacteria and is essential for biofilm formation, biofilm dispersal, and virulence. The alignment of the cell body with the surface during surface swimming impacts bacterial surface sensing. Here, we developed a high-throughput method for characterizing the orientation of the cell body relative to the surface using total internal reflection fluorescence (TIRF) microscopy. The angle between the cell body and the surface was determined by maximizing image cross-correlations between the TIRF image of the cell and a reference library. Utilizing this technique, we surprisingly identified six distinct surface swimming states of Pseudomonas aeruginosa according to the body alignment and the flagellar position. Furthermore, we observed that the near-surface swimming speed is greater in the pull state than in the push state, attributed to hydrodynamic effects near the liquid-solid interface. Hydrodynamic force analysis of the swimming states provided rich insights into the mechanics of bacterial surface swimming. Our technique is readily applicable to the study of surface motility across a wide spectrum of bacterial species.

Transplantation of Endothelial Progenitor Cells Attenuates Lipopolysaccharide-Induced Lung Injury via Inhibiting the Inflammatory Secretion of Neutrophils in Rats.

BACKGROUND: Endothelial progenitor cells (EPCs) are special types of stem cells and are a potential novel therapeutic approach in acute lung injury (ALI). Transplantation of EPCs can ameliorate the inflammatory state by reducing adhesion and exudation of inflammatory cells. However, the mechanism underlying the effect of EPCs on inflammatory response modulation remains unclear. The aim of the present study was to investigate the effect of EPCs on the modulation of neutrophils in vitro and in vivo. MATERIALS AND METHODS: EPCs were cocultured with neutrophils after lipopolysaccharide stimulation in vitro or transplanted into ALI rats, and neutrophil inflammatory mediators including tumor necrosis factor-α, interleukin-1ß, neutrophil elastase, myeloperoxidase and matrix metalloproteinases-9 were detected by enzyme-linked immunosorbent assay, an myeloperoxidase detection kits, reverse transcription-polymerase chain reaction and western blotting. RESULTS: The results showed that EPCs significantly downregulated the expression of inflammatory mediators when cocultured with neutrophils in vitro or in vivo. CONCLUSIONS: These findings demonstrated that EPCs contributed to lung injury in ALI rats by downregulating neutrophil inflammatory mediators.