Heat resistance differences are common between both vegetative cells and spores of type F isolates carrying a chromosomal vs plasmid-borne enterotoxin gene.

type F isolates utilize enterotoxin (CPE) to cause food poisoning (FP) and nonfoodborne gastrointestinal diseases. The enterotoxin gene () can be located on either the chromosome or plasmids, but most FP isolates carry a chromosomal (c) gene. Our 2000 article in (66:3234-3240, 2000, https://doi.

The biology and pathogenicity of type F: a common human enteropathogen with a new(ish) name.

SUMMARYIn the 2018-revised typing classification system, isolates carrying the enterotoxin () and alpha toxin genes but no other typing toxin genes are now designated as type F. Type F isolates cause food poisoning and nonfoodborne human gastrointestinal (GI) diseases, which most commonly involve type F isolates carrying, respectivefooly, a chromosomal or plasmid-borne gene. Compared to spores of other isolates, spores of type F chromosomal isolates often exhibit greater resistance to food environment stresses, likely facilitating their survival in improperly prepared or stored foods.

Overexpressing the Orphan Histidine Kinase Gene in the Absence of Orphan Histidine Kinase Gene Expression, or Vice Versa, Is Sufficient to Obtain Significant Sporulation and Strong Production of Enterotoxin or Spo0A by Type F Strain SM101.

The CPR1953 and CPR1954 orphan histidine kinases profoundly affect sporulation initiation and enterotoxin (CPE) production by type F strain SM101, whether cultured in vitro (modified Duncan-Strong sporulation medium (MDS)) or ex vivo (mouse small intestinal contents (MIC)). To help distinguish whether CPR1953 and CPR1954 act independently or in a stepwise manner to initiate sporulation and CPE production, and null mutants of SM101 were transformed with plasmids carrying the or genes, respectively, causing overexpression of in the absence of expression and vice versa. RT-PCR confirmed that, compared to SM101, the mutant transformed with a plasmid encoding expressed at higher levels while the mutant transformed with a plasmid encoding expressed higher levels of .

The impact of orphan histidine kinases and phosphotransfer proteins on the regulation of clostridial sporulation initiation.

Sporulation is an important feature of the clostridial life cycle, facilitating survival of these bacteria in harsh environments, contributing to disease transmission for pathogenic species, and sharing common early steps that are also involved in regulating industrially important solvent production by some non-pathogenic species. Initial genomics studies suggested that Clostridia lack the classical phosphorelay that phosphorylates Spo0A and initiates sporulation in , leading to the hypothesis that sporulation in Clostridia universally begins when Spo0A is phosphorylated by orphan histidine kinases (OHKs). However, components of the classical phosphorelay were recently identified in some Clostridia.

Identification of orphan histidine kinases that impact sporulation and enterotoxin production by Clostridium perfringens type F strain SM101 in a pathophysiologically-relevant ex vivo mouse intestinal contents model.

When causing food poisoning or antibiotic-associated diarrhea, Clostridium perfringens type F strains must sporulate to produce C. perfringens enterotoxin (CPE) in the intestines. C.

NanJ Is the Major Sialidase for Clostridium perfringens Type F Food Poisoning Strain 01E809.

Clostridium perfringens type F strains cause food poisoning (FP) when they sporulate and produce C. perfringens enterotoxin (CPE) in the intestines. Most type F FP strains carry a chromosomal gene (c- strains).

Epsilon toxin-producing Clostridium perfringens colonize the multiple sclerosis gut microbiome overcoming CNS immune privilege.

Multiple sclerosis (MS) is a complex disease of the CNS thought to require an environmental trigger. Gut dysbiosis is common in MS, but specific causative species are unknown. To address this knowledge gap, we used sensitive and quantitative PCR detection to show that people with MS were more likely to harbor and show a greater abundance of epsilon toxin-producing (ETX-producing) strains of C.

Characterization of NanR Regulation of Sialidase Production, Sporulation and Enterotoxin Production by Type F Strains Carrying a Chromosomal Enterotoxin Gene.

type F food poisoning (FP) strains produce enterotoxin (CPE) to cause a common bacterial food-borne illness in the United States. During FP, CPE is synthesized in the intestines when sporulates. Besides CPE, FP strains also produce sialidases.

Characterizing the Contributions of Various Clostridium perfringens Enterotoxin Properties to and Permeability Effects.

Clostridium perfringens enterotoxin (CPE) is thought to cause lethal enterotoxemia when absorbed from the intestinal lumen into the circulation. CPE action sequentially involves receptor-binding, oligomerization into a prepore, and pore formation. To explore the mechanistic basis by which CPE alters permeability, this study tested the permeability effects of several recombinant CPE (rCPE) species: rCPE and rCPE (which form pores), rC-CPE and rCPE (which bind to receptors but cannot oligomerize), rCPE (which binds and oligomerizes without pore formation), and rCPE (which has poor receptor-binding ability).

Reevaluation of whether a Functional Agr-like Quorum-Sensing System Is Necessary for Production of Wild-Type Levels of Epsilon-Toxin by Clostridium perfringens Type D Strains.

Clostridium perfringens type B and D strains produce epsilon-toxin (ETX). Our 2011 study (mBio 2:e00275-11, 2011, https://doi.org/10.

NanI Sialidase Enhances the Action of Clostridium perfringens Enterotoxin in the Presence of Mucus.

Clostridium perfringens enterotoxin (CPE) is the main virulence factor for C. perfringens type F strains to cause human gastrointestinal diseases, which can involve lethal enterotoxemia. During type F disease, CPE encounters an adherent mucus layer overlying the intestines, so the current study evaluated if NanI potentiates CPE activity in the presence of adherent mucus.

NanI Sialidase Contributes to the Growth and Adherence of Clostridium perfringens Type F Strain F4969 in the Presence of Adherent Mucus.

Clostridium perfringens type F strains causing nonfoodborne human gastrointestinal diseases (NFD) typically produce NanI sialidase as their major secreted sialidase. Type F NFDs can persist for several weeks, indicating their pathogenesis involves intestinal colonization, including vegetative cell growth and adherence, with subsequent sporulation that fosters enterotoxin production and release. We previously reported that NanI contributes to type F NFD strain adherence and growth using Caco-2 cells.

Identifying the Basis for VirS/VirR Two-Component Regulatory System Control of Clostridium perfringens Beta-Toxin Production.

Clostridium perfringens toxin production is often regulated by the Agr-like quorum sensing (QS) system signaling the VirS/VirR two-component regulatory system (TCRS), which consists of the VirS membrane sensor histidine kinase and the VirR response regulator. VirS/VirR is known to directly control expression of some genes by binding to a DNA binding motif consisting of two VirR boxes located within 500 bp of the target gene start codon. Alternatively, the VirS/VirR system can indirectly regulate production levels of other proteins by increasing expression of a small regulatory RNA, VR-RNA.

NanH Is Produced by Sporulating Cultures of Clostridium perfringens Type F Food Poisoning Strains and Enhances the Cytotoxicity of C. perfringens Enterotoxin.

type F food poisoning (FP) strains cause one of the most common foodborne illnesses. This FP develops when type F FP strains sporulate in the intestines and produce enterotoxin (CPE), which is responsible for the diarrhea and abdominal cramps of this disease. While can produce up to three different sialidases, the current study surveyed FP strains, which confirmed the results of a previous study that they consistently carry the sialidase gene, often as their only sialidase gene.

Evidence That VirS Is a Receptor for the Signaling Peptide of the Clostridium perfringens Agr-like Quorum Sensing System.

Since both the Agr (accessory gene regulator)-like quorum sensing (QS) system and VirS/VirR (VirS/R) two-component regulatory system of positively regulate production of several toxins, including beta toxin (CPB), it has been hypothesized the VirS membrane sensor protein is an Agr-like QS signaling peptide (SP) receptor. To begin evaluating whether VirS is an SP receptor, this study sequenced the gene in strains CN3685 and CN1795 because it was reported that mutants of both strains increase CPB production in response to the pentapeptide 5R, likely the natural SP, but only the CN3685 mutant responds to 8R, which is 5R plus a 3-amino-acid tail. This sequencing identified differences between the predicted VirS extracellular loop 2 (ECL2) of CN3685 versus that of CN1795.

Using More Than 1 (Path)Way to Kill a Host Cell: Lessons From Enterotoxin.

enterotoxin (CPE) is responsible for the symptoms of common intestinal infections due to type F isolates. CPE is a pore-forming toxin that uses certain claudins as a receptor. Previous studies showed that, in enterocyte-like Caco-2 cells, low CPE concentrations cause caspase 3-mediated apoptosis but high CPE concentrations cause necrosis.

The Agr-Like Quorum-Sensing System Is Important for Type A Strain ATCC 3624 To Cause Gas Gangrene in a Mouse Model.

type A is involved in gas gangrene in humans and animals. Following a traumatic injury, rapid bacterial proliferation and exotoxin production result in severe myonecrosis. alpha toxin (CPA) and perfringolysin (PFO) are the main virulence factors responsible for the disease.

RIP1, RIP3, and MLKL Contribute to Cell Death Caused by Clostridium perfringens Enterotoxin.

type F strains cause gastrointestinal disease when they produce a pore-forming toxin named enterotoxin (CPE). In human enterocyte-like Caco-2 cells, low CPE concentrations cause caspase-3-dependent apoptosis, while high CPE concentrations cause necrosis. Since necrosis or apoptosis sometimes involves receptor-interacting serine/threonine-protein kinase-1 or 3 (RIP1 or RIP3), this study examined whether those kinases are important for CPE-induced apoptosis or necrosis.

Effects of Claudin-1 on the Action of Enterotoxin in Caco-2 Cells.

enterotoxin (CPE) contributes to diarrhea and an often-lethal enterotoxemia. CPE action starts when it binds to claudin receptors, forming a small complex (90 kDa). Six small complexes then oligomerize to create prepores, followed by insertion of beta-hairpins from CPE to form beta-barrel pores named CH-1 or CH-2.

Identification of an Important Orphan Histidine Kinase for the Initiation of Sporulation and Enterotoxin Production by Type F Strain SM101.

type F strains cause a common human foodborne illness and many cases of nonfoodborne human gastrointestinal diseases. Sporulation plays two critical roles during type F enteric disease. First, it produces broadly resistant spores that facilitate type F strain survival in the food and nosocomial environments.