Evaluation of virulence genes in Proteus strains isolated from diabetic foot infections and urinary tract infections.
Proteus species are frequently isolated from urinary tract infections (UTIs) and diabetic foot infections (DFIs). We aimed to evaluate the presence of virulence genes in P. mirabilis and P. vulgaris strains isolated from DFI and UTI.
A total of 78 Proteus isolates (57 P. mirabilis and 21 P. vulgaris) collected from patients were studied. The isolates were identified using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometer. The presence of virulence-associated genes (hlyA, mrpA, atfA, pmfA, hmpA, ptaA, ureA, ureC, zapA, ireA, rsbA, flaA, and ucaA) was evaluated by polymerase chain reaction (PCR).
46 isolates were obtained from wound cultures, and 32 were obtained from the midstream urine cultures. All virulence genes, except hlyA, were detected in the study. ureA was the most detected gene in both UTI (100%) and DFI isolates (84.8%). The distributions of ureC, flaA, hpmA, ireA, rsbA, pmfA, zapA, ucaA, ptaA, atfA, and mrpA genes in DFI and UTI isolates were as follows: 82.6% and 96.9%, 71.7% and 93.8%, 69.6% and 93.8%, 69.6% and 96.9%, 69.6% and 96.9, 67.4% and 81.3%, 65.2% and 43.8%, 54.3 and 71.9%, 34.8% and 96.9%, 26.1 and 93.8%, and 23.9% and 46.9%, respectively.
We demonstrated that P. mirabilis and P. vulgaris express a variety of virulence genes related to pathogenicity. All virulence genes were found to be more frequent in UTI isolates except zapA. There is limited data on the virulence factors of Proteus species in DFIs. Further studies are needed to investigate virulence genes in wound isolates.
Phiri RM
，Ertuğrul MB
，Bozdoğan B
，Hoşbul T
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《Journal of Infection in Developing Countries》
Unveiling the hidden arsenal: new insights into Proteus mirabilis virulence in UTIs.
Proteus mirabilis is a Gram-negative bacterium commonly found in urinary tract infections (UTIs) and catheter-associated urinary tract infections (CAUTIs). The pathogenic mechanisms of Proteus mirabilis are complex and diverse, involving various virulence factors, including fimbriae, flagella, urease, polyphosphate kinase, lipopolysaccharides, cyclic AMP receptor protein, Sigma factor RpoE, and RNA chaperone protein Hfq. These factors play crucial roles in bacterial colonization, invasion, evasion of host immune responses, biofilm formation, and urinary stone formation. This paper is the first to comprehensively describe the hydrogenase system, autotransporter proteins, molybdate-binding protein ModA, and two-component systems as virulence factors in Proteus mirabilis, providing new insights into its pathogenic mechanisms in urinary tract infections. This review explores the mechanisms of biofilm formation by Proteus mirabilis and the various virulence factors involved in UTIs, revealing many newly discovered virulence factors from recent studies. These findings may offer new targets for clinical treatment of UTIs and vaccine development, highlighting the importance of understanding these virulence factors.
Yang A
，Tian Y
，Li X
《Frontiers in Cellular and Infection Microbiology》
VIM-AS1, which is regulated by CpG methylation, cooperates with IGF2BP1 to inhibit tumor aggressiveness via EPHA3 degradation in hepatocellular carcinoma.
Early tumor recurrence in hepatocellular carcinoma (HCC) remains a challenging area, as the mechanisms involved are not fully understood. While microvascular invasion is linked to early recurrence, established biomarkers for diagnosis and prognostication are lacking. In this study, our objective was to identify DNA methylation sites that can predict the outcomes of liver cancer patients and elucidate the molecular mechanisms driving HCC aggressiveness. Using DNA methylome data from HCC patient samples from the CGRC and TCGA databases, we pinpointed hypermethylated CpG sites in HCC. Our analysis revealed that cg02746869 acts as a crucial regulatory site for VIM-AS1 (vimentin antisense RNA1), a 1.8 kb long noncoding RNA. RNA sequencing of HCC cells with manipulated VIM-AS1 expression revealed EPHA3 as a pathogenic target of VIM-AS1, which performs an oncogenic function in HCC. Hypermethylation-induced suppression of VIM-AS1 significantly impacted HCC cell dynamics, particularly impairing motility and invasiveness. Mechanistically, reduced VIM-AS1 expression stabilized EPHA3 mRNA by enhancing the binding of IGF2BP1 to EPHA3 mRNA, leading to increased expression of EPHA3 mRNA and the promotion of HCC progression. In vivo experiments further confirmed that the VIM-AS1‒EPHA3 axis controlled tumor growth and the tumor microenvironment in HCC. These findings suggest that the downregulation of VIM-AS1 due to hypermethylation at cg02746869 increased EPHA3 mRNA expression via a m6A-dependent mechanism to increase HCC aggressiveness.
Han SH
，Ko JY
，Jung S
，Oh S
，Kim DY
，Kang E
，Kim MS
，Chun KH
，Yoo KH
，Park JH
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ResearchGate
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