The polymerase chain reaction has been used to differentiate the gene which encodes the toxin co-regulated pili (tcpA) of the El Tor and classical biotypes of Vibrio cholerae O1. The same PCR primers were applied to strains belonging to non-O1 serogroups that produced cholera toxin. The size of fragment amplified was either identical to the tcpA of biotype El Tor (471 bp) or to the tcpA of biotype classical (617 bp). All strains belonging to the novel epidemic serogroup O139 generated a 471-bp fragment identical to El Tor tcpA. The present study suggests that there may be an association between non-O1 serogroup and tcpA type.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1574-6968.1995.tb07359.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
VopX, a novel T3SS effector, modulates host actin dynamics.
mBio
January 2025
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.
Unlabelled: Pathogenic strains cause cholera using different mechanisms. O1 and O139 serogroup strains use the toxin-co-regulated pilus (TCP) and cholera toxin (CT) for intestinal colonization and to promote secretory diarrhea, while non-O1/non-O139 serogroup strains are typically non-toxigenic and use alternate virulence factors to cause a clinically similar disease. An O39 serogroup, TCP/CT-negative strain, named AM-19226, uses a type III secretion system (T3SS) to translocate more than 10 effector proteins into the host cell cytosol.
View Article and Find Full Text PDFMeasuring the rate of NADPH consumption by glutathione reductase in the cytosol and mitochondria.
PLoS One
December 2024
Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.
Background: NADPH is an essential co-factor supporting the function of enzymes that participate in both inflammatory and anti-inflammatory pathways in myeloid cells, particularly macrophages. Although individual NADPH-dependent pathways are well characterized, how these opposing pathways are co-regulated to orchestrate an optimized inflammatory response is not well understood. To investigate this, techniques to track the consumption of NADPH need to be applied.
View Article and Find Full Text PDFVibrio cholerae virulence is blocked by chitosan oligosaccharide-mediated inhibition of ChsR activity.
Nat Microbiol
November 2024
National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, People's Republic of China.
Article Synopsis
- Vibrio cholerae is a major cause of cholera, which leads to significant global mortality, and understanding its virulence regulation could pave the way for new treatments.
- The study identifies ChsR, a regulator involved in chitosan utilization, as a factor that enhances V. cholerae virulence by upregulating TcpP, which is crucial for producing cholera toxin.
- Chitosan oligosaccharides were found to inhibit this virulence pathway, and their administration in mice reduced V. cholerae colonization and disease severity, indicating their potential as a therapeutic option for cholera.
Variations in the Antivirulence Effects of Fatty Acids and Virstatin against Strains.
J Microbiol Biotechnol
September 2024
Department of Pharmacy, College of Pharmacy, Hanyang University, Ansan 15588, Republic of Korea.
The expression of two major virulence factors of , cholera toxin (CT) and toxin co-regulated pilus (TCP), is induced by environmental stimuli through a cascade of interactions among regulatory proteins known as the ToxR regulon when the bacteria reach the human small intestine. ToxT is produced via the ToxR regulon and acts as the direct transcriptional activator of CT (), TCP ( gene cluster), and other virulence genes. Unsaturated fatty acids (UFAs) and several small-molecule inhibitors of ToxT have been developed as antivirulence agents against .
View Article and Find Full Text PDFThe ING protein Fng2 associated with RPD3 HDAC complex for the regulation of fungal development and pathogenesis in wheat head blight fungus.
Int J Biol Macromol
May 2024
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production, College of Plant Protection, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address:
Article Synopsis
- * The study identifies the ING protein Fng2 in wheat head blight fungus, revealing that its deletion leads to defects in growth, reproduction, and other critical functions, impacting gene expression significantly.
- * Fng2 negatively regulates histone H4 acetylation and interacts with a histone deacetylase (FgRpd3) to control the expression of thousands of genes, which is essential for fungal development and pathogenicity.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!