The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Horst Posthaus - One of the best experts on this subject based on the ideXlab platform.
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susceptibility of primary human endothelial cells to c perfringens beta toxin suggesting similar pathogenesis in human and porcine Necrotizing Enteritis
Veterinary Microbiology, 2011Co-Authors: Francesca Popescu, Marianne Wyder, Corinne Gurtner, Joachim Frey, R A Cooke, Andrew R Greenhill, Horst PosthausAbstract:Clostridium perfringens type C causes fatal Necrotizing Enteritis in different mammalian hosts, most commonly in newborn piglets. Human cases are rare, but the disease, also called pigbel, was endemic in the Highlands of Papua New Guinea. Lesions in piglets and humans are very similar and characterized by segmental necro-hemorrhagic Enteritis in acute cases and fibrino-Necrotizing Enteritis in subacute cases. Histologically, deep mucosal necrosis accompanied by vascular thrombosis and necrosis was consistently reported in naturally affected pigs and humans. This suggests common pathogenetic mechanisms. Previous in vitro studies using primary porcine aortic endothelial cells suggested that beta-toxin (CPB) induced endothelial damage contributes to the pathogenesis of C. perfringens type C Enteritis in pigs. In the present study we investigated toxic effects of CPB on cultured primary human macro- and microvascular endothelial cells. In vitro, these cells were highly sensitive to CPB and reacted with similar cytopathic and cytotoxic effects as porcine endothelial cells. Our results indicate that porcine and human cell culture based in vitro models represent valuable tools to investigate the pathogenesis of this bacterial disease in animals and humans.
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retrospective study on Necrotizing Enteritis in piglets in switzerland
Schweizer Archiv Fur Tierheilkunde, 2009Co-Authors: M Jaggi, Marianne Wyder, N Wollschlager, Carlos Abril, Sarah Albini, C Brachelente, Horst PosthausAbstract:The re-emergence of Necrotizing Enteritis (NE) in Swiss pig breeding farms raised concern that, besides C. perfringens type C strains, additional C. perfringens toxinotypes might cause this disease. Therefore we retrospectively investigated the association of NE with C. perfringens type C or different C. perfringens toxinotypes. We evaluated pathological lesions, routine diagnostic bacteriology results, and multiplex real-time PCR analyses from DNA extracts of archived intestinal samples of 199 piglets from our diagnostic case load. 96.5 % of NE cases and 100 % of herds affected by NE were positive for C. perfringens type C genotypes. Animals without Necrotizing Enteritis revealed a signifi cantly lower detection rate of type C genotypes. Non affected piglets showed a high prevalence for beta-2-toxin positive C. perfringens type A strains. Collectively, our data indicate that outbreaks of NE in piglets in Switzerland cannot be attributed to newly emerging pathogenic toxinotypes, but are due to a spread of pathogenic C. perfringens type C strains.
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Occurrence of Clostridium perfringens type A and type C in piglets of the Swiss swine population
Schweizer Archiv Fur Tierheilkunde, 2009Co-Authors: N Wollschlager, Horst Posthaus, Sarah Albini, W. Zimmermann, Isabelle Brodard, M. G. Doherr, R. MiserezAbstract:Necrotizing Enteritis (NE) of newborn piglets still represents an economical problem in Swiss pig breeding and production. The aim of our study was to identify risk factors for NE and evaluate the prevalence of C. perfringens with the toxingenes cpb and cpb2 in Swiss pig breeding farms. The prevalence of theses C. perfringens was investigated using fecal swabs followed by bacteriological culturing and genotyping. Close proximity to other breeding farms and large herd sizes were shown to predispose to NE. C. perfringens type C, carrying the genes cpa, cpb and cpb2 were frequently identified in herds with acute outbreaks of NE. Farms not affected by NE or those using prophylactic vaccination against NE were predominantly positive for C. perfringens type A strains with cpb2 and showed much lower prevalence of C. perfringens type C, compared to acutely affected herds. Our results demonstrate that C. perfringens type A strains with cpb2 are not associated with NE. Besides typical necropsy finding, only the identification of cpb can be used for the diagnosis of NE in affected herds.
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clostridium perfringens beta toxin targets endothelial cells in Necrotizing Enteritis in piglets
Veterinary Microbiology, 2009Co-Authors: Julien Miclard, M Jaggi, E Sutter, Marianne Wyder, Benno Grabscheid, Horst PosthausAbstract:Beta-toxin (CPB) is known to be the major virulence factor of Clostridium perfringens type C strains, which cause Necrotizing Enteritis in pigs, sheep, goats, calves, and humans. The exact mode of action, in particular the cellular targets of CPB in the intestine of naturally affected species, is however still not resolved. To investigate localization of CPB in naturally occurring Necrotizing Enteritis, we evaluated 52 piglets with spontaneously acquired C. perfringens type C Enteritis and 14 control animals by immunohistochemistry. Our results consistently revealed binding of CPB to vascular endothelial cells in peracute to acute lesions of Necrotizing Enteritis. Subacute cases, in contrast, demonstrated reduced or no CPB staining at the endothelium, mainly due to widespread vascular necrosis. From these results we conclude, that the pathogenesis of C. perfringens type C induced Necrotizing Enteritis involves binding of CPB to endothelial cells in the small intestine during the early phase of the disease. Thus, by targeting endothelial cells, CPB might specifically induce vascular necrosis, hemorrhage and subsequent hypoxic tissue necrosis.
Kokichi Kikuchi - One of the best experts on this subject based on the ideXlab platform.
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development of multiple Necrotizing Enteritis induced by a tumor necrosis factor like cytokine from lipopolysaccharide stimulated peritoneal macrophages in rats
American Journal of Pathology, 1990Co-Authors: Katsuji Torimoto, Noriyuki Sato, Mamoru Okubo, Atsuhito Yagihashi, Yoshimasa Wada, Isao Hara, H Hayasaka, Kokichi KikuchiAbstract:We report the development of an animal model of multiple Necrotizing Enteritis (MNE) in rats. When rats were injected directly with a culture supernatant of lipopolysaccharide (LPS)-stimulated rat peritoneal macrophages into the abdominal aorta, the overt pathologic lesions of MNE developed within 30 minutes after injection. The rats showed an elevated level of blood fibrinogen degradation product content even 30 minutes after injection. Furthermore the rats that were pretreated intravenously with heparin sulfate did not develop MNE, indicating the acute disturbances of blood microcirculation in the intestine. Multiple Necrotizing Enteritis was developed also by the injection with recombinant tumor necrosis factor (rTNF) but rarely was observed with even a high dose of recombinant interleukin-1 (rIL-1) or platelet-activating factor (PAF). The supernatant was cytotoxic in vitro to TNF-susceptible LM and many other cells but was less cytotoxic to the TNF-resistant LR line. Partial purification of the supernatant suggested that the supernatant contained a cytokine that has biochemical features of TNF. Furthermore polyclonal anti-TNF antibody could inhibit not only the cytotoxicity in vitro but also MNE development in vivo by this factor. These data strongly indicate that MNE possibly could be caused by a TNF-like cytokine produced by macrophages that are stimulated by the endotoxin.
Fumio Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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Necrotizing Enteritis with hepatic portal venous gas and pneumatosis intestinalis report of a case
European Journal of Gastroenterology & Hepatology, 2003Co-Authors: Daisuke Fukumori, Takamitsu Sasaki, Hisanobu Matsumoto, Hitoshi Ohmori, Toru Kakazu, Fumio YamamotoAbstract:: A 73-year-old woman visited our hospital because of increasing abdominal distension and lower abdominal pain. On abdominal computed tomography (CT), hepatic portal venous gas (HPVG) and pneumatosis intestinalis of the small intestine were found. HPVG caused by intestinal necrosis was diagnosed, and an emergency laparotomy was thus performed. Necrosis of the small intestine over a 40-cm area from the ileocaecal region toward the mouth was found, and the lesion was resected. Histopathologically, haemorrhagic necrotic Enteritis was diagnosed. The patient is alive as of the seventieth day after operation. The prognosis of intestinal necrosis accompanied by HPVG and pneumatosis intestinalis is poor. The presence of HPVG suggests the occurrence of a serious lesion in the abdominal cavity. Therefore, appropriate treatment should be performed immediately.
Marianne Wyder - One of the best experts on this subject based on the ideXlab platform.
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susceptibility of primary human endothelial cells to c perfringens beta toxin suggesting similar pathogenesis in human and porcine Necrotizing Enteritis
Veterinary Microbiology, 2011Co-Authors: Francesca Popescu, Marianne Wyder, Corinne Gurtner, Joachim Frey, R A Cooke, Andrew R Greenhill, Horst PosthausAbstract:Clostridium perfringens type C causes fatal Necrotizing Enteritis in different mammalian hosts, most commonly in newborn piglets. Human cases are rare, but the disease, also called pigbel, was endemic in the Highlands of Papua New Guinea. Lesions in piglets and humans are very similar and characterized by segmental necro-hemorrhagic Enteritis in acute cases and fibrino-Necrotizing Enteritis in subacute cases. Histologically, deep mucosal necrosis accompanied by vascular thrombosis and necrosis was consistently reported in naturally affected pigs and humans. This suggests common pathogenetic mechanisms. Previous in vitro studies using primary porcine aortic endothelial cells suggested that beta-toxin (CPB) induced endothelial damage contributes to the pathogenesis of C. perfringens type C Enteritis in pigs. In the present study we investigated toxic effects of CPB on cultured primary human macro- and microvascular endothelial cells. In vitro, these cells were highly sensitive to CPB and reacted with similar cytopathic and cytotoxic effects as porcine endothelial cells. Our results indicate that porcine and human cell culture based in vitro models represent valuable tools to investigate the pathogenesis of this bacterial disease in animals and humans.
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retrospective study on Necrotizing Enteritis in piglets in switzerland
Schweizer Archiv Fur Tierheilkunde, 2009Co-Authors: M Jaggi, Marianne Wyder, N Wollschlager, Carlos Abril, Sarah Albini, C Brachelente, Horst PosthausAbstract:The re-emergence of Necrotizing Enteritis (NE) in Swiss pig breeding farms raised concern that, besides C. perfringens type C strains, additional C. perfringens toxinotypes might cause this disease. Therefore we retrospectively investigated the association of NE with C. perfringens type C or different C. perfringens toxinotypes. We evaluated pathological lesions, routine diagnostic bacteriology results, and multiplex real-time PCR analyses from DNA extracts of archived intestinal samples of 199 piglets from our diagnostic case load. 96.5 % of NE cases and 100 % of herds affected by NE were positive for C. perfringens type C genotypes. Animals without Necrotizing Enteritis revealed a signifi cantly lower detection rate of type C genotypes. Non affected piglets showed a high prevalence for beta-2-toxin positive C. perfringens type A strains. Collectively, our data indicate that outbreaks of NE in piglets in Switzerland cannot be attributed to newly emerging pathogenic toxinotypes, but are due to a spread of pathogenic C. perfringens type C strains.
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clostridium perfringens beta toxin targets endothelial cells in Necrotizing Enteritis in piglets
Veterinary Microbiology, 2009Co-Authors: Julien Miclard, M Jaggi, E Sutter, Marianne Wyder, Benno Grabscheid, Horst PosthausAbstract:Beta-toxin (CPB) is known to be the major virulence factor of Clostridium perfringens type C strains, which cause Necrotizing Enteritis in pigs, sheep, goats, calves, and humans. The exact mode of action, in particular the cellular targets of CPB in the intestine of naturally affected species, is however still not resolved. To investigate localization of CPB in naturally occurring Necrotizing Enteritis, we evaluated 52 piglets with spontaneously acquired C. perfringens type C Enteritis and 14 control animals by immunohistochemistry. Our results consistently revealed binding of CPB to vascular endothelial cells in peracute to acute lesions of Necrotizing Enteritis. Subacute cases, in contrast, demonstrated reduced or no CPB staining at the endothelium, mainly due to widespread vascular necrosis. From these results we conclude, that the pathogenesis of C. perfringens type C induced Necrotizing Enteritis involves binding of CPB to endothelial cells in the small intestine during the early phase of the disease. Thus, by targeting endothelial cells, CPB might specifically induce vascular necrosis, hemorrhage and subsequent hypoxic tissue necrosis.
Qiaoli Yang - One of the best experts on this subject based on the ideXlab platform.
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circular rna expression profile of spleen in a clostridium perfringens type c induced piglet model of Necrotizing Enteritis
FEBS Open Bio, 2018Co-Authors: Tiantuan Jiang, Pengfei Wang, Xiaoyu Huang, Qiaoli YangAbstract:: Clostridium perfringens type C is a pathogen that causes Necrotizing Enteritis (NE), which is an intestinal tract disease in piglets. The pathogenesis of C. perfringens type C-induced NE is still unclear, leading to a lack of effective therapies. Earlier studies have reported that circular RNAs (circRNAs) are involved in the pathogenic processes of various diseases. However, it is not known if circRNAs in spleen play a role in C. perfringens type C infection in NE. To address this question, we infected 7-day-old piglets with C. perfringens type C to induce NE. Hematoxylin and eosin staining of small intestine revealed inflammation, atrophy and shedding of intestinal villi, and intestinal mucosal necrosis. We observed increased expression of cytokine genes (such as IL-1β and IL-6) and inflammation in the spleen. In addition, we used RNA-seq and bioinformatics analysis to examine changes in circRNA expression. A total of 103 circRNAs were found to be differentially expressed in NE, and Gene Ontology analysis revealed that the genes producing differentially expressed circRNAs were enriched in regulation of the cellular metabolic process protein binding. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the genes producing differentially expressed circRNAs were involved in the tumor necrosis factor signaling pathway, T cell receptor signaling pathway and nuclear factor-κB signaling pathway. Finally, we found eight circRNAs (including circ_0002220 and circ_0000821) that are related to NE. Therefore, our study provides new insights into the mechanisms underlying C. perfringens type C infection in piglets.
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Circular RNA expression profile of spleen in a Clostridium perfringens type C‐induced piglet model of Necrotizing Enteritis
FEBS Open Bio, 2018Co-Authors: Tiantuan Jiang, Pengfei Wang, Xiaoyu Huang, Qiaoli YangAbstract:Clostridium perfringens type C is a pathogen that causes Necrotizing Enteritis (NE), which is an intestinal tract disease in piglets. The pathogenesis of C. perfringens type C‐induced NE is still unclear, leading to a lack of effective therapies. Earlier studies have reported that circular RNAs (circRNAs) are involved in the pathogenic processes of various diseases. However, it is not known if circRNAs in spleen play a role in C. perfringens type C infection in NE. To address this question, we infected 7‐day‐old piglets with C. perfringens type C to induce NE. Hematoxylin and eosin staining of small intestine revealed inflammation, atrophy and shedding of intestinal villi, and intestinal mucosal necrosis. We observed increased expression of cytokine genes (such as IL‐1β and IL‐6) and inflammation in the spleen. In addition, we used RNA‐seq and bioinformatics analysis to examine changes in circRNA expression. A total of 103 circRNAs were found to be differentially expressed in NE, and Gene Ontology analysis revealed that the genes producing differentially expressed circRNAs were enriched in regulation of the cellular metabolic process protein binding. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the genes producing differentially expressed circRNAs were involved in the tumor necrosis factor signaling pathway, T cell receptor signaling pathway and nuclear factor‐κB signaling pathway. Finally, we found eight circRNAs (including circ_0002220 and circ_0000821) that are related to NE. Therefore, our study provides new insights into the mechanisms underlying C. perfringens type C infection in piglets.
