The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform

Karla J. F. Satchell - One of the best experts on this subject based on the ideXlab platform.

  • Additive Function of vibrio vulnificus martxvv and vvha cytolysins promotes rapid growth and epithelial tissue necrosis during intestinal infection
    PLOS Pathogens, 2012
    Co-Authors: Hee Gon Jeong, Karla J. F. Satchell
    Abstract:

    Vibrio vulnificus is a pathogen that causes both severe necrotizing wound infections and life-threatening food-borne infections. Food-borne infection is particularly lethal as the infection can progress rapidly to primary septicemia resulting in death from septic shock and multiorgan failure. In this study, we use both bioluminescence whole animal imaging and V. vulnificus bacterial colonization of orally infected mice to demonstrate that the secreted multiFunctional-autoprocessing RTX toxin (MARTXVv) and the cytolysin/hemolysin VvhA of clinical isolate CMCP6 have an important Function in the gut to promote early in vivo growth and dissemination of this pathogen from the small intestine to other organs. Using histopathology, we find that both cytotoxins can cause villi disruption, epithelial necrosis, and inflammation in the mouse small intestine. A double mutant deleted of genes for both cytotoxins was essentially avirulent, did not cause intestinal epithelial tissue damage, and was cleared from infected mice by 36 hours by an effective immune response. Therefore, MARTXVv and VvhA seem to play an Additive role for pathogenesis of CMCP6 causing intestinal tissue damage and inflammation that then promotes dissemination of the infecting bacteria to the bloodstream and other organs. In the absence of these two secreted factors, we propose that this bacterium is unable to cause intestinal infection in humans.

  • correction Additive Function of vibrio vulnificus martx vv and vvha cytolysins promotes rapid growth and epithelial tissue necrosis during intestinal infection
    PLOS Pathogens, 2012
    Co-Authors: Hee Gon Jeong, Karla J. F. Satchell
    Abstract:

    Vibrio vulnificus is a pathogen that causes both severe necrotizing wound infections and life-threatening food-borne infections. Food-borne infection is particularly lethal as the infection can progress rapidly to primary septicemia resulting in death from septic shock and multiorgan failure. In this study, we use both bioluminescence whole animal imaging and V. vulnificus bacterial colonization of orally infected mice to demonstrate that the secreted multiFunctional-autoprocessing RTX toxin (MARTXVv) and the cytolysin/hemolysin VvhA of clinical isolate CMCP6 have an important Function in the gut to promote early in vivo growth and dissemination of this pathogen from the small intestine to other organs. Using histopathology, we find that both cytotoxins can cause villi disruption, epithelial necrosis, and inflammation in the mouse small intestine. A double mutant deleted of genes for both cytotoxins was essentially avirulent, did not cause intestinal epithelial tissue damage, and was cleared from infected mice by 36 hours by an effective immune response. Therefore, MARTXVv and VvhA seem to play an Additive role for pathogenesis of CMCP6 causing intestinal tissue damage and inflammation that then promotes dissemination of the infecting bacteria to the bloodstream and other organs. In the absence of these two secreted factors, we propose that this bacterium is unable to cause intestinal infection in humans.

Hee Gon Jeong - One of the best experts on this subject based on the ideXlab platform.

  • Additive Function of vibrio vulnificus martxvv and vvha cytolysins promotes rapid growth and epithelial tissue necrosis during intestinal infection
    PLOS Pathogens, 2012
    Co-Authors: Hee Gon Jeong, Karla J. F. Satchell
    Abstract:

    Vibrio vulnificus is a pathogen that causes both severe necrotizing wound infections and life-threatening food-borne infections. Food-borne infection is particularly lethal as the infection can progress rapidly to primary septicemia resulting in death from septic shock and multiorgan failure. In this study, we use both bioluminescence whole animal imaging and V. vulnificus bacterial colonization of orally infected mice to demonstrate that the secreted multiFunctional-autoprocessing RTX toxin (MARTXVv) and the cytolysin/hemolysin VvhA of clinical isolate CMCP6 have an important Function in the gut to promote early in vivo growth and dissemination of this pathogen from the small intestine to other organs. Using histopathology, we find that both cytotoxins can cause villi disruption, epithelial necrosis, and inflammation in the mouse small intestine. A double mutant deleted of genes for both cytotoxins was essentially avirulent, did not cause intestinal epithelial tissue damage, and was cleared from infected mice by 36 hours by an effective immune response. Therefore, MARTXVv and VvhA seem to play an Additive role for pathogenesis of CMCP6 causing intestinal tissue damage and inflammation that then promotes dissemination of the infecting bacteria to the bloodstream and other organs. In the absence of these two secreted factors, we propose that this bacterium is unable to cause intestinal infection in humans.

  • correction Additive Function of vibrio vulnificus martx vv and vvha cytolysins promotes rapid growth and epithelial tissue necrosis during intestinal infection
    PLOS Pathogens, 2012
    Co-Authors: Hee Gon Jeong, Karla J. F. Satchell
    Abstract:

    Vibrio vulnificus is a pathogen that causes both severe necrotizing wound infections and life-threatening food-borne infections. Food-borne infection is particularly lethal as the infection can progress rapidly to primary septicemia resulting in death from septic shock and multiorgan failure. In this study, we use both bioluminescence whole animal imaging and V. vulnificus bacterial colonization of orally infected mice to demonstrate that the secreted multiFunctional-autoprocessing RTX toxin (MARTXVv) and the cytolysin/hemolysin VvhA of clinical isolate CMCP6 have an important Function in the gut to promote early in vivo growth and dissemination of this pathogen from the small intestine to other organs. Using histopathology, we find that both cytotoxins can cause villi disruption, epithelial necrosis, and inflammation in the mouse small intestine. A double mutant deleted of genes for both cytotoxins was essentially avirulent, did not cause intestinal epithelial tissue damage, and was cleared from infected mice by 36 hours by an effective immune response. Therefore, MARTXVv and VvhA seem to play an Additive role for pathogenesis of CMCP6 causing intestinal tissue damage and inflammation that then promotes dissemination of the infecting bacteria to the bloodstream and other organs. In the absence of these two secreted factors, we propose that this bacterium is unable to cause intestinal infection in humans.

Snorri S Thorgeirsson - One of the best experts on this subject based on the ideXlab platform.

  • coexpression of flt 3 ligand flt 3 and scf c kit signal transduction system in bile duct ligated si and w mice
    American Journal of Pathology, 1997
    Co-Authors: M Omori, N Omori, Ritva P Evarts, Tadahisa Teramoto, Snorri S Thorgeirsson
    Abstract:

    Stem cell factor (SCF) and its receptor c-kit constitute an important signal transduction system regulating cell growth and differentiation in hematopoiesis, gametogenesis, and melanogenesis. Recently, we have demonstrated that both SCF and c-kit are expressed in the bile duct epithelial cells of the rat liver and are highly up-regulated during activation of the normally dormant hepatic stem cell compartment. In the present study, we used sl/sld and w/wv mice, which have mutation of either SCF or c-kit, to study the possible involvement of the SCF/c-kit system in the bile duct proliferation. Bile duct ligation was performed to induce the proliferation of bile duct epithelial cells. The transcripts for both SCF and c-kit were clearly increased after bile duct ligation in both control and mutant mice. Moreover, both Sl and W mice responded to the bile duct ligation, similar to the control mice, by developing new bile ducts. Recently, a novel tyrosine kinase receptor, flt-3 receptor, has been identified in the fetal liver. It has been reported that the flt-3 ligand (FL)/flt-3 system can synergize with the SCF/c-kit system and stimulate the proliferation of hematopoietic cells. Therefore, we hypothesized that the FL/flt-3 system might compensate for the compromised SCF/c-kit system in the liver of Sl and W mice. The expression of both FL and flt-3 were significantly increased in bile duct-ligated liver from both normal and mutant mice, and the transcripts for the flt-3 receptor were selectively located on bile duct epithelial cells. Based on these results, we postulate the existence of a compensatory/Additive Function between the FL/flt-3 and the SCF/c-kit signal transduction systems in hepatic cell biology.

Joachim Wipper - One of the best experts on this subject based on the ideXlab platform.

M Omori - One of the best experts on this subject based on the ideXlab platform.

  • coexpression of flt 3 ligand flt 3 and scf c kit signal transduction system in bile duct ligated si and w mice
    American Journal of Pathology, 1997
    Co-Authors: M Omori, N Omori, Ritva P Evarts, Tadahisa Teramoto, Snorri S Thorgeirsson
    Abstract:

    Stem cell factor (SCF) and its receptor c-kit constitute an important signal transduction system regulating cell growth and differentiation in hematopoiesis, gametogenesis, and melanogenesis. Recently, we have demonstrated that both SCF and c-kit are expressed in the bile duct epithelial cells of the rat liver and are highly up-regulated during activation of the normally dormant hepatic stem cell compartment. In the present study, we used sl/sld and w/wv mice, which have mutation of either SCF or c-kit, to study the possible involvement of the SCF/c-kit system in the bile duct proliferation. Bile duct ligation was performed to induce the proliferation of bile duct epithelial cells. The transcripts for both SCF and c-kit were clearly increased after bile duct ligation in both control and mutant mice. Moreover, both Sl and W mice responded to the bile duct ligation, similar to the control mice, by developing new bile ducts. Recently, a novel tyrosine kinase receptor, flt-3 receptor, has been identified in the fetal liver. It has been reported that the flt-3 ligand (FL)/flt-3 system can synergize with the SCF/c-kit system and stimulate the proliferation of hematopoietic cells. Therefore, we hypothesized that the FL/flt-3 system might compensate for the compromised SCF/c-kit system in the liver of Sl and W mice. The expression of both FL and flt-3 were significantly increased in bile duct-ligated liver from both normal and mutant mice, and the transcripts for the flt-3 receptor were selectively located on bile duct epithelial cells. Based on these results, we postulate the existence of a compensatory/Additive Function between the FL/flt-3 and the SCF/c-kit signal transduction systems in hepatic cell biology.