causes multiple diseases in humans and animals. Its pathogenic effect is supported by a broad and heterogeneous arsenal of toxins and other virulence factors associated with a specific host tropism. Molecular approaches have indicated that most toxins produce membrane pores, leading to osmotic cell disruption and apoptosis. However, identifying mechanisms involved in cell tropism and selective toxicity effects should be studied more. The differential presence and polymorphisms of toxin-encoding genes and genes encoding other virulence factors suggest that molecular mechanisms might exist associated with host preference, receptor binding, and impact on the host; however, this information has not been reviewed in detail. Therefore, this review aims to clarify the current state of knowledge on the structural features and mechanisms of action of the major toxins and virulence factors of discuss the impact of genetic diversity of toxinotypes in tropism for several hosts.
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http://dx.doi.org/10.1080/22221751.2024.2341968 | DOI Listing |
The combined use of lytic bacteriophages with antibiotics is currently being explored as a strategy to enhance the effectiveness of infectious disease therapies, including those caused by . In this study, we investigated the synergistic potential of bacteriophage vB_SauM-515A1 ( family) and the first-line antibiotic linezolid against the methicillin-resistant strain SA0413Rev. A checkerboard assay revealed a significant synergistic effect against planktonic cells (FIC = 0.
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December 2024
Ningxia Key Laboratory of Clinical and Pathogenic Microbiology, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China.
The global prevalence of ST11 hypervirulent carbapenem-resistant (hv-CRKP) isolates has been increasingly documented, yet genomic characterization of this clone remains insufficiently explored. Here, we report a clinical ST11-KL25 hv-CRKP strain (KP156) that exhibited resistance to multiple antibiotics and demonstrated hypervirulence in a mouse infection model. Whole-genome sequencing revealed that KP156 harbored one virulence plasmid (pKP156-Vir) and two resistance plasmids (pKP156-KPC and pKP156-tetA).
View Article and Find Full Text PDFCell Surf
June 2025
Department of Biology, College of Natural and Computational Science, Mekdela Amba University, P.O. Box 32, Tulu Awuliya, Ethiopia.
has evolved a sophisticated regulatory system to control its virulence. One of the main roles of this interconnected network is to sense and respond to diverse environmental signals by altering the synthesis of virulence components required for survival in the host, including cell surface adhesins, extracellular enzymes and toxins. The accessory gene regulator (agr), a quorum sensing system that detects the local concentration of a cyclic peptide signaling molecule, is one of the well-studied of these .
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January 2025
College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China; Jilin Province Sika Deer Efficient Breeding and Product Development Technology Engineering Research Center, Changchun, China; The Ministry of Education Key Laboratory of Animal Production and the Product Quality and Safety, Changchun, China. Electronic address:
Mycobacterium tuberculosis enters the body through the respiratory tract, produces and releases virulence proteins through a variety of mechanisms, regulates the host immune mechanism through a variety of ways, and then survives in the body for a long time. These depend on virulence genes encoded by Mycobacterium tuberculosis. Previous studies found that the Rv3435c gene of Mycobacterium tuberculosis is highly conserved in pathogenic mycobacterium, but not conserved in non-pathogenic mycobacterium, which may be a potential virulence gene, and inhibit the secretion of inflammatory factors in RAW264.
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December 2024
College of Integrated Traditional Chinese and Western Medicine, Changchun University of Chinese Medicine, Changchun 130117, China. Electronic address:
A medical predicament has led to extensive drug resistance in methicillin-resistant Staphylococcus aureus (MRSA), and the complexity of treatment has increased exponentially with the induction of osteomyelitis. In view of the severe situation and the potential of bacterial antivirulence strategies, this study focused on the key virulence factor caseinolytic protease (ClpP) of S. aureus to identify new strategies against MRSA-induced osteomyelitis.
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