Cronobacter sakazakii is an opportunistic pathogen that has been implicated in meningitis, NEC, and sepsis in neonates. Colonization and subsequent infection and invasion of C. sakazakii require that the organism adheres to host cell surfaces. Agents that inhibit or block attachment of the pathogen to epithelial cells could be useful in reducing infections. The goal of this research was to assess the ability of prebiotic galactooligosaccharides (GOS) and polydextrose (PDX) to inhibit adherence of C. sakazakii 4603 to a HEp-2 human cell line. Adherence experiments were performed in the presence or absence of prebiotics using HEp-2 cells grown to confluency on glass coverslips. Prebiotics and bacteria were added and incubated for 3 h. Coverslips were washed, and adherence was determined by cultural and microscopic methods. When measured microscopically or by cultural methods, significant reductions in adherence (56 and 71%, respectively) of C. sakazakii were observed in the presence of GOS (16 mg/ml). Adherence inhibition also occurred (48%) when a GOS-PDX blend (8 mg/ml each) was tested, although PDX by itself had less effect. Similar results were also observed for Caco-2 cells and also for another strain of C. sakazakii (29004). These results suggest that GOS and PDX, alone and in combination, may have an anti-adhesive effect on C. sakazakii and directly inhibit the adherence to gastrointestinal epithelial cells.
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http://dx.doi.org/10.1007/s00284-011-9882-8 | DOI Listing |
Bull Exp Biol Med
January 2025
Hunan University of Chinese Medicine, Changsha, Hunan, China.
We studied the effect of acteoside on a model of human corneal epithelial cells (HCEC) injury induced by HO. HCEC were divided into 4 groups and cultured for 24 h in normal medium (intact and control groups, respectively), or in a medium containing DMSO or 160 μM acteoside (DMSO and acteoside groups, respectively). Then, HO solution was added to HCEC for 4 h, except for intact cells.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Emergency Medicine, Institute of Disaster Medicine and Institute of Emergency Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, 610041, People's Republic of China.
Background: A significant association between immune cells and sepsis has been suggested by observational studies. However, the precise biological mechanisms underlying this association remain unclear. Therefore, we employed a Mendelian randomization (MR) approach to investigate the causal relationship between immune cells and genetic susceptibility to sepsis, and to explore the potential mediating role of blood metabolites.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Genetics, Yale School of Medicine, New Haven, CT, USA.
Skin epithelial stem cells correct aberrancies induced by oncogenic mutations. Oncogenes invoke different strategies of epithelial tolerance; while wild-type cells outcompete β-catenin-gain-of-function (βcatGOF) cells, Hras cells outcompete wild-type cells. Here we ask how metabolic states change as wild-type stem cells interface with mutant cells and drive different cell-competition outcomes.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Nephrology, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: The pathogenesis of acute kidney injury (AKI) is not fully understood. Tax1-binding protein 1 (TAX1BP1) modulates inflammation and apoptosis through the NF-kB signaling pathway, however, its specific role in ischemic AKI remains unclear.
Methods: We injected a TAX1BP1 overexpression plasmid into the tail vein of male C57BL/6 mice, followed by clamping the bilateral renal arteries to induce AKI.
Sci Rep
January 2025
Department of Pathology and Laboratory Medicine, Collage of Medicine, the University of Tennessee Health Science Center, Memphis, TN, 38163, United States.
Deoxyhypusine synthase (DHPS) is an enzyme encoded by the DHPS gene, with high expression in various cancers, including ovarian cancer (OC). DHPS regulates the translation initiation factor EIF5A, and EIF5A2 knockout inhibits OC tumor growth and metastasis by blocking the epithelial-to-mesenchymal transition (EMT) and the TGFβ pathway. In this study, we show that DHPS is amplified in OC patients, and its elevated expression correlates with poor survival.
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