Enteropathogenic Escherichia coli
Critical role of T cell-dependent serum antibody, but not the gut-associated lymphoid tissue, for surviving acute mucosal infection with Citrobacter rodentium, an attaching and effacing pathogen. (1/177)Citrobacter rodentium uses virulence factors similar to the enteropathogenic Escherichia coli to produce attaching and effacing lesions in the distal colon of mice. We used this infection model to determine components of adaptive immunity needed to survive infection. During acute infection, wild-type mice develop breaks across infected epithelial surfaces but resolve infection. Surprisingly, mice markedly deficient in mucosal lymphocyte populations from beta(7) integrin deficiency resolve infection, as do CD8alpha-/- or TCR-delta-/- mice. In contrast, CD4-/- or TCR-beta-/- mice develop polymicrobial sepsis and end-organ damage, and succumb during acute infection, despite epithelial damage similar to wild-type mice. B cell-deficient (MuMT-/-) or B and T cell-deficient (recombinase-activating gene 2-/-) mice develop severe pathology in colon and internal organs, and deteriorate rapidly during acute infection. Surviving mice develop robust Citrobacter-specific serum IgM responses during acute infection, whereas mice that succumb do not. However, CD4-/- mice receiving serum Igs from infected wild-type mice survive and clear the infection. Our data show that survival of apparently self-limited and luminal mucosal infections requires a systemic T cell-dependent Ab response against bacteria that enter through damaged mucosa. These findings have implications for understanding host defense against mucosal infections, including the pathogenesis of these diseases in immunocompromised populations. (+info)
Dissecting virulence: systematic and functional analyses of a pathogenicity island. (2/177)Bacterial pathogenicity islands (PAI) often encode both effector molecules responsible for disease and secretion systems that deliver these effectors to host cells. Human enterohemorrhagic Escherichia coli (EHEC), enteropathogenic E. coli, and the mouse pathogen Citrobacter rodentium (CR) possess the locus of enterocyte effacement (LEE) PAI. We systematically mutagenized all 41 CR LEE genes and functionally characterized these mutants in vitro and in a murine infection model. We identified 33 virulence factors, including two virulence regulators and a hierarchical switch for type III secretion. In addition, 7 potential type III effectors encoded outside the LEE were identified by using a proteomics approach. These non-LEE effectors are encoded by three uncharacterized PAIs in EHEC O157, suggesting that these PAIs act cooperatively with the LEE in pathogenesis. Our findings provide significant insights into bacterial virulence mechanisms and disease. (+info)
Identification of a novel Citrobacter rodentium type III secreted protein, EspI, and roles of this and other secreted proteins in infection. (3/177)Citrobacter rodentium is a member of a group of pathogens that colonize the lumen of the host gastrointestinal tract via attaching and effacing (A/E) lesion formation. C. rodentium, which causes transmissible colonic hyperplasia in mice, is used as an in vivo model system for the clinically significant A/E pathogens enterohemorrhagic and enteropathogenic Escherichia coli. These bacteria all contain a pathogenicity island called the locus of enterocyte effacement (LEE), which encodes a type III secretion system that is designed to deliver effector proteins into eukaryotic host cells. These effectors are involved in the subversion of host eukaryotic cell functions to the benefit of the bacterium. In this study we used mutant strains to determine the effects of the C. rodentium LEE-encoded effectors EspF, EspG, EspH, and Map on virulence in the mouse model. In addition, we identified a novel secreted protein, EspI encoded outside the LEE, whose secretion is also dependent on a functional type III secretion system. Mutant strains with each of the effectors investigated were found to be outcompeted by wild-type bacteria in mixed-infection experiments in vivo, although the effects of EspF and EspH were only subtle. In single-infection experiments, we found that EspF, EspG, and EspH are not required for efficient colonization of the mouse colon or for the production of hyperplasia. In contrast, strains producing EspI and Map had significant colonization defects and resulted in dramatically reduced levels of hyperplasia, and they exhibited very different growth dynamics in mice than the wild-type strain exhibited. (+info)
Clearance of Citrobacter rodentium requires B cells but not secretory immunoglobulin A (IgA) or IgM antibodies. (4/177)Citrobacter rodentium, a murine model pathogen for human enteropathogenic Escherichia coli, predominantly colonizes the lumen and mucosal surface of the colon and cecum and causes crypt hyperplasia and mucosal inflammation. Mice infected with C. rodentium develop a secretory immunoglobulin A (IgA) response, but the role of B cells or secretory antibodies in host defense is unknown. To address this question, we conducted oral C. rodentium infections in mice lacking B cells, IgA, secreted IgM, polymeric Ig receptor (pIgR), or J chain. Normal mice showed peak bacterial numbers in colon and feces at 1 week and bacterial eradication after 3 to 4 weeks. B-cell-deficient mice were equally susceptible initially but could not control infection subsequently. Tissue responses showed marked differences, as infection of normal mice was accompanied by transient crypt hyperplasia and mucosal inflammation in the colon and cecum at 2 but not 6 weeks, whereas B-cell-deficient mice had few mucosal changes at 2 weeks but severe epithelial hyperplasia with ulcerations and mucosal inflammation at 6 weeks. The functions of B cells were not mediated by secretory antibodies, since mice lacking IgA or secreted IgM or proteins required for their transport into the lumen, pIgR or J chain, cleared C. rodentium normally. Nonetheless, systemic administration of immune sera reduced bacterial numbers significantly in normal and pIgR-deficient mice, and depletion of IgG abrogated this effect. These results indicate that host defense against C. rodentium depends on B cells and IgG antibodies but does not require production or transepithelial transport of IgA or secreted IgM. (+info)
Protective role of arginase in a mouse model of colitis. (5/177)Arginase is the endogenous inhibitor of inducible NO synthase (iNOS), because both enzymes use the same substrate, l-arginine (Arg). Importantly, arginase synthesizes ornithine, which is metabolized by the enzyme ornithine decarboxylase (ODC) to produce polyamines. We investigated the role of these enzymes in the Citrobacter rodentium model of colitis. Arginase I, iNOS, and ODC were induced in the colon during the infection, while arginase II was not up-regulated. l-Arg supplementation of wild-type mice or iNOS deletion significantly improved colitis, and l-Arg treatment of iNOS(-/-) mice led to an additive improvement. There was a significant induction of IFN-gamma, IL-1, and TNF-alpha mRNA expression in colitis tissues that was markedly attenuated with l-Arg treatment or iNOS deletion. Treatment with the arginase inhibitor S-(2-boronoethyl)-l-cysteine worsened colitis in both wild-type and iNOS(-/-) mice. Polyamine levels were increased in colitis tissues, and were further increased by l-Arg. In addition, in vivo inhibition of ODC with alpha-difluoromethylornithine also exacerbated the colitis. Taken together, these data indicate that arginase is protective in C. rodentium colitis by enhancing the generation of polyamines in addition to competitive inhibition of iNOS. Modulation of the balance of iNOS and arginase, and of the arginase-ODC metabolic pathway may represent a new strategy for regulating intestinal inflammation. (+info)
Macroscopic, microscopic and biochemical characterisation of spontaneous colitis in a transgenic mouse, deficient in the multiple drug resistance 1a gene. (6/177)1 A novel animal model of spontaneous colonic inflammation, the multiple drug-resistant (mdr1) a(-/-) mouse, was identified by Panwala and colleagues in 1998. The aim of our study was to further characterise this model, specifically by measuring cytokines that have been implicated in inflammatory bowel disease (IBD) (IL-8 and IFN-gamma) in the colon/rectum of mdr1a(-/-) mice, and by determining the sensitivity of these, together with the macroscopic, microscopic and disease signs of colitis, to dexamethasone (0.05, 0.3 and 2 mg kg(-1) subcutaneously (s.c.) daily for 7 days). 2 All mdr1a(-/-) mice had microscopic evidence of inflammation in the caecum and colon/rectum, while control mice with the same genetic background did not. Significant increases in colon/rectum and caecal weights and also in cytokine levels (both IFN-gamma and IL-8) in homogenised colon/rectum were observed in mdr1a(-/-) mice compared to mdr1a(+/+) mice. 3 Dexamethasone reduced the increases in tissue weights and also microscopic grading of colitis severity, but had no effect on IFN-gamma or IL-8. 4 This study supports the similarity of the gastrointestinal inflammation present in mdr1a(-/-) mice to that of human IBD, in particular Crohn's disease. This has been demonstrated at the macroscopic and microscopic levels, and was supported further by elevations in colonic levels of IFN-gamma and IL-8 and the disease signs observed. The incidence of colitis was much higher than previously reported, with all mice having microscopic evidence of colitis. The limited variance between animals in the parameters measured suggests that this model is reproducible. (+info)
Impaired immunity to intestinal bacterial infection in stromelysin-1 (matrix metalloproteinase-3)-deficient mice. (7/177)Infection of mice with the intestinal bacterial pathogen Citrobacter rodentium results in colonic mucosal hyperplasia and a local Th1 inflammatory response similar to that seen in mouse models of inflammatory bowel disease. Matrix metalloproteinases (MMPs) have been shown to mediate matrix remodeling and cell migration during tissue injury and repair in the intestine. We have previously shown enhanced pathology in infected TNFRp55-/-, IL-12p40-/-, and IFN-gamma-/- mice, and here we show that this is associated with an increase in stromelysin-1 (MMP3) transcripts in colonic tissues. We have therefore investigated the role of MMP3 in colonic mucosal hyperplasia and the local Th1 responses using MMP3-/- mice. In MMP3-/- mice, similar mucosal thickening was observed after infection as in wild-type (WT) mice. Colonic tissues from MMP3-/- mice showed a compensatory increase in the expression of other MMP transcripts, such as MMP7 and MMP12. However, MMP3-/- mice showed delayed clearance of bacteria and delayed appearance of CD4+ T lymphocytes into intestinal lamina propria. CSFE-labeled mesenteric lymph node CD4+ T lymphocytes from infected WT mice migrated in fewer numbers into the mesenteric lymph nodes and colon of MMP3-/- mice than into those of WT mice. These studies show that mucosal remodeling can occur in the absence of MMP3, but that MMP3 plays a role in the migration of CD4+ T lymphocytes to the intestinal mucosa. (+info)
EspJ is a prophage-carried type III effector protein of attaching and effacing pathogens that modulates infection dynamics. (8/177)Enterohemorrhagic Escherichia coli, enteropathogenic E. coli, and Citrobacter rodentium are highly adapted enteropathogens that successfully colonize their host's gastrointestinal tract via the formation of attaching and effacing (A/E) lesions. These pathogens utilize a type III secretion system (TTSS) apparatus, encoded by the locus of enterocyte effacement, to translocate bacterial effector proteins into epithelial cells. Here, we report the identification of EspJ (E. coli-secreted protein J), a translocated TTSS effector that is carried on the 5' end of the cryptic prophage CP-933U. Infection of epithelial cells in culture revealed that EspJ is not required for A/E lesion activity in vivo and ex vivo. However, in vivo studies performed with mice demonstrated that EspJ possesses properties that influence the dynamics of clearance of the pathogen from the host's intestinal tract, suggesting a role in host survival and pathogen transmission. (+info)
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The most common type of colitis is ulcerative colitis, which affects the rectum and lower part of the colon. The symptoms of ulcerative colitis can include:
* Diarrhea (which may be bloody)
* Abdominal pain and cramping
* Rectal bleeding
* Weight loss
* Loss of appetite
* Nausea and vomiting
Microscopic colitis is another type of colitis that is characterized by inflammation in the colon, but without visible ulcers or bleeding. The symptoms of microscopic colitis are similar to those of ulcerative colitis, but may be less severe.
Other types of colitis include:
* Infantile colitis: This is a rare condition that affects babies and young children, and is characterized by diarrhea, fever, and vomiting.
* Isomorphic colitis: This is a rare condition that affects the colon and rectum, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Radiation colitis: This is a condition that occurs after radiation therapy to the pelvic area, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Ischemic colitis: This is a condition where there is a reduction in blood flow to the colon, which can lead to inflammation and symptoms such as abdominal pain and diarrhea.
The diagnosis of colitis typically involves a combination of physical examination, medical history, and diagnostic tests such as:
* Colonoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the colon and rectum.
* Endoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the esophagus, stomach, and duodenum.
* Stool tests: These are tests that analyze stool samples for signs of inflammation or infection.
* Blood tests: These are tests that analyze blood samples for signs of inflammation or infection.
* Biopsy: This is a test that involves taking a small sample of tissue from the colon and examining it under a microscope for signs of inflammation or infection.
Treatment for colitis depends on the underlying cause, but may include medications such as:
* Aminosalicylates: These are medications that help to reduce inflammation in the colon and relieve symptoms such as diarrhea and abdominal pain. Examples include sulfasalazine (Azulfidine) and mesalamine (Asacol).
* Corticosteroids: These are medications that help to reduce inflammation in the body. They may be used short-term to control acute flares of colitis, or long-term to maintain remission. Examples include prednisone and hydrocortisone.
* Immunomodulators: These are medications that help to suppress the immune system and reduce inflammation. Examples include azathioprine (Imuran) and mercaptopurine (Purinethol).
* Biologics: These are medications that target specific proteins involved in the inflammatory response. Examples include infliximab (Remicade) and adalimumab (Humira).
In addition to medication, lifestyle changes such as dietary modifications and stress management techniques may also be helpful in managing colitis symptoms. Surgery may be necessary in some cases where the colitis is severe or persistent, and involves removing damaged portions of the colon and rectum.
It's important to note that colitis can increase the risk of developing colon cancer, so regular screening for colon cancer is recommended for people with chronic colitis. Additionally, people with colitis may be more susceptible to other health problems such as osteoporosis, osteopenia, and liver disease, so it's important to work closely with a healthcare provider to monitor for these conditions and take steps to prevent them.
1. Ulcerative colitis: This is a chronic condition that causes inflammation and ulcers in the colon. Symptoms can include abdominal pain, diarrhea, and rectal bleeding.
2. Crohn's disease: This is a chronic condition that affects the digestive tract, including the colon. Symptoms can include abdominal pain, diarrhea, fatigue, and weight loss.
3. Irritable bowel syndrome (IBS): This is a common condition characterized by recurring abdominal pain, bloating, and changes in bowel movements.
4. Diverticulitis: This is a condition where small pouches form in the colon and become inflamed. Symptoms can include fever, abdominal pain, and changes in bowel movements.
5. Colon cancer: This is a type of cancer that affects the colon. Symptoms can include blood in the stool, changes in bowel movements, and abdominal pain.
6. Inflammatory bowel disease (IBD): This is a group of chronic conditions that cause inflammation in the digestive tract, including the colon. Symptoms can include abdominal pain, diarrhea, fatigue, and weight loss.
7. Rectal cancer: This is a type of cancer that affects the rectum, which is the final portion of the colon. Symptoms can include blood in the stool, changes in bowel movements, and abdominal pain.
8. Anal fissures: These are small tears in the skin around the anus that can cause pain and bleeding.
9. Rectal prolapse: This is a condition where the rectum protrudes through the anus. Symptoms can include rectal bleeding, pain during bowel movements, and a feeling of fullness or pressure in the rectal area.
10. Hemorrhoids: These are swollen veins in the rectum or anus that can cause pain, itching, and bleeding.
It's important to note that some of these conditions can be caused by other factors as well, so if you're experiencing any of these symptoms, it's important to see a doctor for an accurate diagnosis and treatment.
1. Hantavirus pulmonary syndrome (HPS): This is a severe respiratory disease caused by the hantavirus, which is found in the urine and saliva of infected rodents. Symptoms of HPS can include fever, headache, muscle pain, and difficulty breathing.
2. Leptospirosis: This is a bacterial infection caused by the bacterium Leptospira, which is found in the urine of infected rodents. Symptoms can include fever, headache, muscle pain, and jaundice (yellowing of the skin and eyes).
3. Rat-bite fever: This is a bacterial infection caused by the bacterium Streptobacillus moniliformis, which is found in the saliva of infected rodents. Symptoms can include fever, headache, muscle pain, and swollen lymph nodes.
4. Lymphocytic choriomeningitis (LCM): This is a viral infection caused by the lymphocytic choriomeningitis virus (LCMV), which is found in the urine and saliva of infected rodents. Symptoms can include fever, headache, muscle pain, and meningitis (inflammation of the membranes surrounding the brain and spinal cord).
5. Tularemia: This is a bacterial infection caused by the bacterium Francisella tularensis, which is found in the urine and saliva of infected rodents. Symptoms can include fever, headache, muscle pain, and swollen lymph nodes.
These are just a few examples of the many diseases that can be transmitted to humans through contact with rodents. It is important to take precautions when handling or removing rodents, as they can pose a serious health risk. If you suspect that you have been exposed to a rodent-borne disease, it is important to seek medical attention as soon as possible.
There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:
1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.
The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:
* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain
Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.
AP-1 transcription factor
Type three secretion system
List of MeSH codes (B03)
Innate lymphoid cell
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In vivo bioluminescence imaging of the murine pathogen Citrobacter rodentium - PubMed
Transcriptional frameshifting rescues Citrobacter rodentium Type VI secretion by the production of two length variants from the...
Gammaproteobacteria - Citrobacter rodentium | CU Experts | CU Boulder
Epithelial phosphatidylinositol-3-kinase signaling is required for ß-catenin activation and host defense against Citrobacter...
Psidium guajava leaf extract prevents intestinal colonization of Citrobacter rodentium in the mouse model<...
PmrC (EptA) and CptA Negatively Affect Outer Membrane Vesicle Production in Citrobacter rodentium - RIIP - Réseau...
Relationship between intestinal microbiota and colorectal cancer
Project : USDA ARS
Natural remedies for Crohn's: Supplements, oils, and more
Infection trains the host for microbiota-enhanced resistance to pathogens - PubMed
The Hai Ning Shi Lab at Mass General Hospital
Slimy partners: the mucus barrier and gut microbiome in ulcerative colitis | Experimental & Molecular Medicine
Frontiers | Stress, Dietary Patterns and Cardiovascular Disease: A Mini-Review
Induction and prevention of gastric cancer with combined Helicobacter pylori and capsaicin administration and DFMO treatment,...
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FAB: 24 April 2017 - Futurity - These gut microbes may protect babies from infections
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RCSB PDB - 4R72: Structure of the periplasmic binding protein AfuA from Actinobacillus pleuropneumoniae (apo form)
EPIGENOMIC CONTROL OF ANTIMICROBIAL IMMUNITY IN THE INTESTINE | National Agricultural Library
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Profound Implications of the Virome for Human Health and Autoimmunity | One Radio Network
Grant Abstract: Role of stress-induced reduction in Lactobacillus reuteri on colonic inflammation
General PCr(Phosphocreatine) ELISA Kit - The GKTS : Group Kinesitherapy Work Scoliosis.
- Citrobacter rodentium is a natural mouse pathogen related to enteropathogenic and enterohemorrhagic Escherichia coli. (nih.gov)
- In addition, BLI revealed that C. rodentium colonizes the rectum, a site previously unreported for this pathogen. (nih.gov)
- Citrobacter rodentium, a common mouse pathogen, is known to mimic the pathogenecity of enteropathogenic and enterohemorrhagic E. coli. (cmich.edu)
- Our group has previously shown that PmrC (also known as EptA) and CptA maintain OM integrity and provide resistance to iron toxicity and antibiotics in the murine pathogen Citrobacter rodentium In several enteric bacteria, these proteins modify the lipid A and core regions of lipopolysaccharide with phosphoethanolamine moieties. (archives-ouvertes.fr)
- 8. Interleukin-7 produced by intestinal epithelial cells in response to Citrobacter rodentium infection plays a major role in innate immunity against this pathogen. (nih.gov)
- 9. MyD88 signalling plays a critical role in host defence by controlling pathogen burden and promoting epithelial cell homeostasis during Citrobacter rodentium-induced colitis. (nih.gov)
- 12. Impaired resistance and enhanced pathology during infection with a noninvasive, attaching-effacing enteric bacterial pathogen, Citrobacter rodentium, in mice lacking IL-12 or IFN-gamma. (nih.gov)
- Upon oral challenge with the murine colonic pathogen Citrobacter rodentium, which induces colonic histopathology with similarities to human IBD, mice exposed to SDR (and thus having lower levels of L. reuteri) had a significant increase in pathogen-induced colitis as indicated by a significant increase in colonic histopathology, chemokines (e.g. (nih.gov)
- Increased numbers of P-ß- catenin (552)-stained epithelial cells were found throughout expanded crypts in C. rodentium colitis . (bvsalud.org)
- The anthocyanin malvidin alleviated the murine colitis induced by Citrobacter rodentium. (usda.gov)
- 3. Preinoculation with the probiotic Lactobacillus acidophilus early in life effectively inhibits murine Citrobacter rodentium colitis. (nih.gov)
- 4. CD4+ T cells transfer resistance against Citrobacter rodentium-induced infectious colitis by induction of Th 1 immunity. (nih.gov)
- 14. Saccharomyces boulardii ameliorates Citrobacter rodentium-induced colitis through actions on bacterial virulence factors. (nih.gov)
- Importantly, preventing the stressor-induced reduction in L. reuteri by feeding L. reuteri to the mice during stressor exposure abrogated the effects of the stressor on C. rodentium-induced colitis. (nih.gov)
- Thus, the use of C. rodentium is an ideal model to determine whether the colonic epithelium is critical in the link between stress, the microbiota, and exacerbation of colitis. (nih.gov)
- We recently found that IL-21 is necessary to optimize activation of interferon-stimulated genes (ISGs) in gut CD4 T cells to effectively clear a Citrobacter rodentium colitis. (nih.gov)
- Citrobacter rodentium infection of mice induces cell -mediated immune responses associated with crypt hyperplasia and epithelial ß- catenin signaling. (bvsalud.org)
- C57BL/6 mice were infected with C. rodentium and treated with dimethyl sulfoxide ( DMSO ) (vehicle control) or with the PI3K inhibitor LY294002 or wortmannin . (bvsalud.org)
- In response to C. rodentium infection, 5,123 probe sets were differentially expressed in one or both lines of mice. (nih.gov)
- Electrolyte analysis revealed reduction in serum levels of chloride and sodium in susceptible animals.The results support the hypothesis that mortality in C. rodentium-infected susceptible mice is associated with impaired intestinal ion transport and development of fatal fluid loss and dehydration. (nih.gov)
- 7. Citrobacter rodentium infection causes iNOS-independent intestinal epithelial dysfunction in mice. (nih.gov)
- 15. Impaired innate immune response and enhanced pathology during Citrobacter rodentium infection in mice lacking functional P-selectin. (nih.gov)
- 18. Citrobacter rodentium of mice and man. (nih.gov)
- But when the researchers added bacteria from 16-day-old normal mice, the amount of C. rodentium in the guts of surviving mice went down. (fabresearch.org)
- They exposed groups of these mice to C. rodentium and found that only the mice given Clostridia were able to resist the infections. (fabresearch.org)
- Our studies demonstrate that stressor-induced reduction in commensal Lactobacillus reuteri is involved with the observed increase in colonic histopathology in mice challenged with Citrobacter rodentium during exposure to a well characterized and widely used social stressor. (nih.gov)
- General Information: Citrobacter rodentium is the causative agent of transmissible murine colonic hyperplasia in mice. (up.ac.za)
- 2. The natural cytotoxicity receptor NKp46 is dispensable for IL-22-mediated innate intestinal immune defense against Citrobacter rodentium. (nih.gov)
- 10. Citrobacter rodentium infection causes both mitochondrial dysfunction and intestinal epithelial barrier disruption in vivo: role of mitochondrial associated protein (Map). (nih.gov)
- Research in the Shi lab has shown that helminth co-infection results in an impaired host protection and the development of more severe C. rodentium -mediated intestinal inflammation by a STAT 6 (Th2) dependent mechanism. (massgeneral.org)
- These data suggest a novel mechanism by which C. rodentium and possibly other Gram-negative bacteria can negatively affect OMV production through the PmrAB-regulated genes pmrC (eptA) and cptAIMPORTANCE Although OMVs secreted by Gram-negative bacteria fulfill multiple functions, the molecular mechanism of OMV biogenesis remains ill defined. (archives-ouvertes.fr)
- Here, we show that these proteins also repress OMV production in response to environmental iron in C. rodentium These data support the emerging understanding that lipopolysaccharide modifications are important regulators of OMV biogenesis in Gram-negative bacteria. (archives-ouvertes.fr)
- They tried it again with Citrobacter rodentium , a strain of bacteria similar to the E. coli strains that make humans sick. (fabresearch.org)
- We show that the inhibition of PI3K signaling attenuates epithelial Akt activation, the Ser552 phosphorylation and activation of ß- catenin , and epithelial cell proliferative responses during C. rodentium infection . (bvsalud.org)
- Epithelial phosphatidylinositol-3-kinase signaling is required for ß-catenin activation and host defense against Citrobacter rodentium infection. (bvsalud.org)
- C. rodentium ΔafuA was significantly impaired in an in vivo murine competitive assay as well as its ability to transmit infection from an afflicted to a naïve murine host. (rcsb.org)
- C. rodentium are being used as models for studying mucosal response to infection, colon tumor production, and virulence associated with pathogenic E. coli. (up.ac.za)
- This system involves two murine enteric infectious agents that induce distinct Th responses: (i) the helminth Heligmosomoides polygyrus (Th2) and (ii) the Gram-negative bacterium Citrobacter rodentium (Th1). (massgeneral.org)
- AfuABC is conserved across a wide range of bacterial genera, including the enteric pathogens EHEC O157:H7 and its murine-specific relative Citrobacter rodentium, where it lies adjacent to genes implicated in sugar sensing and acquisition. (rcsb.org)
- We have previously utilized bioluminescence imaging (BLI) to determine the in vivo colonization dynamics of C. rodentium. (nih.gov)
- However, due to the oxygen requirement of the bioluminescence system and the colonic localization of C. rodentium, in vivo localization studies were performed using harvested organs. (nih.gov)
- Here, we report the detection of bioluminescent C. rodentium and commensal E. coli during colonization of the gastrointestinal tract in intact living animals. (nih.gov)
- Like its human homologue (i.e., enteropathogenic E. coli), C. rodentium induces colonic inflammation by colonizing the colonic epithelium. (nih.gov)
- Importantly, plasmid complementation of C. rodentium strains with either pmrC (eptA) or cptA resulted in a drastic inhibition of OMV production. (archives-ouvertes.fr)
- Compared to the wild type, the C. rodentium ΔpmrAB strain exhibited heightened OMV production at similar iron concentrations. (archives-ouvertes.fr)
- 13. Emergence of a 'hyperinfectious' bacterial state after passage of Citrobacter rodentium through the host gastrointestinal tract. (nih.gov)
- In the present study, the P. guajava leaf extract was tested for its efficacy in treating infectious diarrhea using a C. rodentium mouse model. (cmich.edu)
- Our aim was to determine whether epithelial PI3K/Akt activation is required for ß- catenin signaling and host defense against C. rodentium. (bvsalud.org)
- The results suggest that the host defense against C. rodentium requires epithelial PI3K activation to induce Akt-mediated ß- catenin signaling and the clearance of C. rodentium independent of adaptive immune responses . (bvsalud.org)
- In Citrobacter rodentium, the tssM1 gene does not encode the C-terminal domain. (ucc.ie)
- Gueguen E, Wills NM, Atkins JF, Cascales E (2014) Transcriptional Frameshifting Rescues Citrobacter rodentium Type VI Secretion by the Production of Two Length Variants from the Prematurely Interrupted tssM Gene. (ucc.ie)
- In wild-type Citrobacter rodentium, the presence of increasing subtoxic concentrations of iron was found to stimulate OMV production 4- to 9-fold above baseline. (archives-ouvertes.fr)
- C. rodentium uses the two-component system PmrAB to sense and adapt to environmental iron. (archives-ouvertes.fr)
- Like its human homologue (i.e., enteropathogenic E. coli), C. rodentium induces colonic inflammation by colonizing the colonic epithelium. (nih.gov)
- Attaching and effacing pathogens include enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC, respectively) and Citrobacter rodentium ( 1 , 2 ). (cdc.gov)