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Virulence Dec 2024The genus includes human, animal, insect, and plant pathogens as well as many symbionts and harmless bacteria. Within this genus are and the complex, with four human... (Review)
Review
The genus includes human, animal, insect, and plant pathogens as well as many symbionts and harmless bacteria. Within this genus are and the complex, with four human pathogenic species that are highly related at the genomic level including the causative agent of plague, . Extensive laboratory, field work, and clinical research have been conducted to understand the underlying pathogenesis and zoonotic transmission of these pathogens. There are presently more than 500 whole genome sequences from which an evolutionary footprint can be developed that details shared and unique virulence properties. Whereas the virulence of now seems in apparent homoeostasis within its flea transmission cycle, substantial evolutionary changes that affect transmission and disease severity continue to ndergo apparent selective pressure within the other that cause intestinal diseases. In this review, we will summarize the present understanding of the virulence and pathogenesis of , highlighting shared mechanisms of virulence and the differences that determine the infection niche and disease severity.
Topics: Animals; Humans; Yersinia; Virulence; Yersinia pestis; Plague; Yersinia Infections
PubMed: 38389313
DOI: 10.1080/21505594.2024.2316439 -
Clinics in Laboratory Medicine Jun 2015Salmonella, Shigella, and Yersinia cause a well-characterized spectrum of disease in humans, ranging from asymptomatic carriage to hemorrhagic colitis and fatal... (Review)
Review
Salmonella, Shigella, and Yersinia cause a well-characterized spectrum of disease in humans, ranging from asymptomatic carriage to hemorrhagic colitis and fatal typhoidal fever. These pathogens are responsible for millions of cases of food-borne illness in the United States each year, with substantial costs measured in hospitalizations and lost productivity. In the developing world, illness caused by these pathogens is not only more prevalent but also associated with a greater case-fatality rate. Classic methods for identification rely on selective media and serology, but newer methods based on mass spectrometry and polymerase chain reaction show great promise for routine clinical testing.
Topics: Bacteriological Techniques; Classification; Dysentery, Bacillary; Humans; Microbial Sensitivity Tests; Salmonella; Salmonella Infections; Shigella; Specimen Handling; Yersinia; Yersinia Infections
PubMed: 26004640
DOI: 10.1016/j.cll.2015.02.002 -
Frontiers in Cellular and Infection... 2023Increasing attention is being paid to the unique roles gut microbes play in both physiological and pathological processes. Crohn's disease (CD) is a chronic, relapsing,... (Review)
Review
Increasing attention is being paid to the unique roles gut microbes play in both physiological and pathological processes. Crohn's disease (CD) is a chronic, relapsing, inflammatory disease of the gastrointestinal tract with unknown etiology. Currently, gastrointestinal infection has been proposed as one initiating factor of CD. , a zoonotic pathogen that exists widely in nature, is one of the most common bacteria causing acute infectious gastroenteritis, which displays clinical manifestations similar to CD. However, the specific role of in CD is controversial. In this Review, we discuss the current knowledge on how and derived microbial compounds may link to the pathogenesis of CD. We highlight examples of -targeted interventions in the diagnosis and treatment of CD, and provide perspectives for future basic and translational investigations on this topic.
Topics: Humans; Crohn Disease; Yersinia enterocolitica; Gastrointestinal Diseases; Yersinia Infections
PubMed: 36968108
DOI: 10.3389/fcimb.2023.1129996 -
F1000Research 2019The human and animal pathogens , which causes bubonic and pneumonic plague, and and , which cause gastroenteritis, share a type 3 secretion system which injects... (Review)
Review
The human and animal pathogens , which causes bubonic and pneumonic plague, and and , which cause gastroenteritis, share a type 3 secretion system which injects effector proteins, Yops, into host cells. This system is critical for virulence of all three pathogens in tissue infection. Neutrophils are rapidly recruited to infected sites and all three pathogens frequently interact with and inject Yops into these cells during tissue infection. Host receptors, serum factors, and bacterial adhesins appear to collaborate to promote neutrophil- interactions in tissues. The ability of neutrophils to control infection is mixed depending on the stage of infection and points to the efficiency of Yops and other bacterial factors to mitigate bactericidal effects of neutrophils. in close proximity to neutrophils has higher levels of expression from promoters, and neutrophils in close proximity to express higher levels of pro-survival genes than migrating neutrophils. In infected tissues, YopM increases neutrophil survival and YopH targets a SKAP2/SLP-76 signal transduction pathway. Yet the full impact of these and other Yops and other factors on neutrophils in infected tissues has yet to be understood.
Topics: Adhesins, Bacterial; Animals; Bacterial Outer Membrane Proteins; Gene Expression Regulation, Bacterial; Humans; Neutrophils; Yersinia; Yersinia Infections
PubMed: 31327994
DOI: 10.12688/f1000research.18940.1 -
Frontiers in Cellular and Infection... 2012Among the seventeen species of the Gram-negative genus Yersinia, three have been shown to be virulent and pathogenic to humans and animals-Y. enterocolitica, Y.... (Review)
Review
Among the seventeen species of the Gram-negative genus Yersinia, three have been shown to be virulent and pathogenic to humans and animals-Y. enterocolitica, Y. pseudotuberculosis, and Y. pestis. In order to be so, they are armoured with various factors that help them adhere to tissues and organelles, cross the cellular barrier and escape the immune system during host invasion. The group of proteins that mediate pathogen-host interactions constitute adhesins. Invasin, Ail, YadA, YadB, YadC, Pla, and pH 6 antigen belong to the most prominent and best-known Yersinia adhesins. They act at different times and stages of infection complementing each other by their ability to bind a variety of host molecules such as collagen, fibronectin, laminin, β1 integrins, and complement regulators. All the proteins are anchored in the bacterial outer membrane (OM), often forming rod-like or fimbrial-like structures that protrude to the extracellular milieu. Structural studies have shown that the anchor region forms a β-barrel composed of 8, 10, or 12 antiparallel β-strands. Depending on the protein, the extracellular part can be composed of several domains belonging to the immunoglobulin fold superfamily, or form a coiled-coil structure with globular head domain at the end, or just constitute several loops connecting individual β-strands in the β-barrel. Those extracellular regions define the activity of each adhesin. This review focuses on the structure and function of these important molecules, and their role in pathogenesis.
Topics: Adhesins, Bacterial; Animals; Bacterial Adhesion; Humans; Models, Biological; Models, Molecular; Protein Conformation; Virulence Factors; Yersinia Infections; Yersinia enterocolitica; Yersinia pestis; Yersinia pseudotuberculosis
PubMed: 23316485
DOI: 10.3389/fcimb.2012.00169 -
Nature Microbiology Apr 2023Granulomas are organized immune cell aggregates formed in response to chronic infection or antigen persistence. The bacterial pathogen Yersinia pseudotuberculosis (Yp)...
Granulomas are organized immune cell aggregates formed in response to chronic infection or antigen persistence. The bacterial pathogen Yersinia pseudotuberculosis (Yp) blocks innate inflammatory signalling and immune defence, inducing neutrophil-rich pyogranulomas (PGs) within lymphoid tissues. Here we uncover that Yp also triggers PG formation within the murine intestinal mucosa. Mice lacking circulating monocytes fail to form defined PGs, have defects in neutrophil activation and succumb to Yp infection. Yersinia lacking virulence factors that target actin polymerization to block phagocytosis and reactive oxygen burst do not induce PGs, indicating that intestinal PGs form in response to Yp disruption of cytoskeletal dynamics. Notably, mutation of the virulence factor YopH restores PG formation and control of Yp in mice lacking circulating monocytes, demonstrating that monocytes override YopH-dependent blockade of innate immune defence. This work reveals an unappreciated site of Yersinia intestinal invasion and defines host and pathogen drivers of intestinal granuloma formation.
Topics: Animals; Mice; Monocytes; Yersinia Infections; Yersinia pseudotuberculosis Infections; Yersinia pseudotuberculosis; Virulence Factors; Granuloma
PubMed: 36879169
DOI: 10.1038/s41564-023-01338-6 -
Frontiers in Cellular and Infection... 2016Hallmarks of Yersinia pathogenesis include the ability to form biofilms on surfaces, the ability to establish close contact with eukaryotic target cells and the ability... (Review)
Review
Hallmarks of Yersinia pathogenesis include the ability to form biofilms on surfaces, the ability to establish close contact with eukaryotic target cells and the ability to hijack eukaryotic cell signaling and take over control of strategic cellular processes. Many of these virulence traits are already well-described. However, of equal importance is knowledge of both confined and global regulatory networks that collaborate together to dictate spatial and temporal control of virulence gene expression. This review has the purpose to incorporate historical observations with new discoveries to provide molecular insight into how some of these regulatory mechanisms respond rapidly to environmental flux to govern tight control of virulence gene expression by pathogenic Yersinia.
Topics: Adaptation, Physiological; Amino Acids; Biofilms; Biological Transport; Carbohydrate Metabolism; Gene Expression Regulation, Bacterial; Humans; Hydrogen-Ion Concentration; Iron; Quorum Sensing; RNA, Bacterial; RNA, Small Untranslated; Signal Transduction; Stress, Physiological; Temperature; Yersinia; Yersinia Infections
PubMed: 26973818
DOI: 10.3389/fcimb.2016.00025 -
BioMed Research International 2020Endoscopy is currently the gold standard for the diagnosis of inflammatory bowel disease (IBD). The presence of macroscopic lesions along with the microscopic detection... (Review)
Review
Endoscopy is currently the gold standard for the diagnosis of inflammatory bowel disease (IBD). The presence of macroscopic lesions along with the microscopic detection of inflammatory infiltration in the terminal ileum often leads the gastroenterologist to the diagnosis of Crohn's disease (CD). However, some of these cases could be, in fact, an infection caused by spp., accompanied or not with CD, which could be easily diagnosed with the identification of serum antibodies against outer protein antigens (YOP antigens). Since Yersiniosis is considered to be an uncommon situation, food and water are not usually checked for the possibility of contamination by . Therefore, it is reasonable to assume that the true prevalence of infection in patients with terminal ileitis is probably underestimated. In this article, we review the most important data regarding the various aspects of infection with special focus on its pathophysiology and diagnosis. We recommend testing for serum antibodies against YOP antigens in all patients with an endoscopic and histological image of terminal ileitis in order to identify Yersiniosis in conjunction or not with terminal ileum CD.
Topics: Adult; Child; Child, Preschool; Crohn Disease; Humans; Middle Aged; Yersinia; Yersinia Infections
PubMed: 32566652
DOI: 10.1155/2020/1240626 -
International Journal of Infectious... May 2016The aim of this study was to exploit the extensive database on strains of Yersinia collected over more than 50 years in France in order to gain an overview of... (Review)
Review
OBJECTIVES
The aim of this study was to exploit the extensive database on strains of Yersinia collected over more than 50 years in France in order to gain an overview of yersiniosis and potential sources of contamination in this country.
METHODS
The 19 670 strains of Yersinia of human, animal, environmental, and food origin isolated in France were grouped by species, biotype, and serotype.
RESULTS
Most human strains (59%) were pathogenic, with a marked predominance of Yersinia enterocolitica bioserotype 4/O:3 (66.8%), followed by Y. enterocolitica 2/O:9 (23.8%) and Yersinia pseudotuberculosis (6.1%). Pigs and pork meat were the nearly exclusive sources of Y. enterocolitica 4/O:3. Other pathogenic strains were rarely isolated from food or environmental samples (0.2%). The major source of pathogenic Yersinia was the animal reservoir, with a remarkable association between Y. enterocolitica 4/O:3 and pigs, Y. pseudotuberculosis and wildlife, Y. enterocolitica 2/O:9 and grazing farm animals, Y. enterocolitica 5/O:2,3 and hares, and Y. enterocolitica 3/O:1,2,3 and chinchillas.
CONCLUSIONS
The frequency of human infection caused by certain Yersinia subgroups might be related to the frequency of exposure to specific animal sources. In contrast, non-pathogenic Yersinia were commonly isolated from foodstuffs and the environment, most probably accounting for the abundance of non-pathogenic Yersinia recovered from human stools.
Topics: Animals; Databases, Factual; Environment; Feces; France; Humans; Red Meat; Swine; Yersinia Infections; Yersinia enterocolitica; Yersinia pseudotuberculosis; Yersinia pseudotuberculosis Infections
PubMed: 26987478
DOI: 10.1016/j.ijid.2016.03.008 -
Frontiers in Cellular and Infection... 2012Cell death plays a central role in host-pathogen interactions, as it can eliminate the pathogen's replicative niche and provide pro-inflammatory signals necessary for an... (Review)
Review
Cell death plays a central role in host-pathogen interactions, as it can eliminate the pathogen's replicative niche and provide pro-inflammatory signals necessary for an effective immune response; conversely, cell death can allow pathogens to eliminate immune cells and evade anti-microbial effector mechanisms. In response to developmental signals or cell-intrinsic stresses, the executioner caspases-3 and -7 mediate apoptotic cell death, which is generally viewed as immunologically silent or immunosuppressive. A proinflammatory form of cell death that requires caspase-1, termed pyroptosis, is activated in response to microbial products within the host cytosol or disruption of cellular membranes by microbial pathogens. Infection by the bacterial pathogen Yersinia has features of both apoptosis and pyroptosis. Cell death and caspase-1 processing in Yersinia-infected cells occur in response to inhibition of NF-κB and MAPK signaling by the Yersinia virulence factor YopJ. However, the molecular basis of YopJ-induced cell death, and the role of different death pathways in anti-Yersinia immune responses remain enigmatic. Here, we discuss the role that cell death may play in inducing specific pro-inflammatory signals that shape innate and adaptive immune responses against Yersinia infection.
Topics: Animals; Caspase 1; Cell Death; Host-Pathogen Interactions; Humans; Signal Transduction; Yersinia; Yersinia Infections
PubMed: 23226685
DOI: 10.3389/fcimb.2012.00149