Staphylococcus epidermidis has become a serious nosocomial pathogen frequently causing infections associated with implanted foreign materials. Biofilm formation is considered a major factor determining S. epidermidis pathogenicity in such device-associated infections. Here, evidence is presented that extracellular DNA is important for the initial phase of biofilm development by S. epidermidis on polystyrene or glass surfaces under static or hydrodynamic conditions. Comparative PCR amplification from S. epidermidis chromosomal and extracellular DNA indicated that the extracellular DNA is similar to chromosomal DNA. Experiments involving the S. epidermidis wild-type and an isogenic atlE mutant indicated that most of the extracellular DNA in S. epidermidis cultures and biofilms is generated through activity of the autolysin AtlE. The presented results suggest that extracellular DNA is generated in S. epidermidis populations through AtlE-mediated lysis of a subpopulation of the bacteria, and that the extracellular DNA promotes biofilm formation of the remaining population.
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http://dx.doi.org/10.1099/mic.0.2007/006031-0 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305.
Exercising regularly promotes health, but these benefits are complicated by acute inflammation induced by exercise. A potential source of inflammation is cell-free DNA (cfDNA), yet the cellular origins, molecular causes, and immune system interactions of exercise-induced cfDNA are unclear. To study these, 10 healthy individuals were randomized to a 12-wk exercise program of either high-intensity tactical training (HITT) or traditional moderate-intensity training (TRAD).
View Article and Find Full Text PDFMicrobial pathogens generate extracellular vesicles (EVs) for intercellular communication and quorum sensing. Microbial EVs also induce inflammatory pathways within host innate immune cells. We previously demonstrated that EVs secreted by trigger type I interferon signaling in host cells specifically via the cGAS-STING innate immune signaling pathway.
View Article and Find Full Text PDFJHEP Rep
January 2025
Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Background & Aims: The role of infiltrating neutrophils in hepatocellular carcinoma (HCC) is modulated by cellular metabolism, specifically lipid homeostasis. Throughout the progression of HCC, alterations in lipid metabolism are intricately linked with regulation of neutrophil function and the release of neutrophil extracellular traps (NETs). However, how much the protumor effect of a high-fat diet (HFD) depends on NETs and the potential interplay between NETs and other leukocytes in HCC remains uncertain.
View Article and Find Full Text PDFJ Recept Signal Transduct Res
January 2025
Department of Pharmaceutical Sciences, Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, USA.
The proliferative effects of angiotensin (Ang) II in vascular smooth muscle cells (VSMCs) through its ability to stimulate extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathway have been established. The main goal of this study was to explore whether Ang III induces ERK1/2 MAPK and VSMC proliferation in cultured Wistar VSMCs. Further, the Ang III actions were compared to those observed in VSMCs derived from the spontaneously hypertensive rat (SHR).
View Article and Find Full Text PDFAnim Genet
February 2025
Department of Clinical Sciences and Services, Centre for Vaccinology and Regenerative Medicine, The Royal Veterinary College, Hatfield, Herts, UK.
Bone fractures are a significant problem in Thoroughbred racehorses. The risk of fracture is influenced by both genetic and environmental factors. To determine the biological processes that are affected in genetically susceptible horses, we utilised polygenic risk scoring to establish induced pluripotent stem cells (iPSCs) from horses at high and low genetic risk.
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