Requirement for TNF-Tnfrsf1 signalling for sclerosing cholangitis in mice chronically infected by<i>Cryptosporidium parvum</i>

Ponnuraj, Esther M.; Hayward, Anthony R.

doi:10.1046/j.1365-2249.2002.01861.x

Cited by 20 publications

(6 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…38 In animal models, TNFα-Tnfrsf1 signaling was important for development of sclerosing cholangitis in a chronic infection with cryptosporidium parvum. 39 Thus, it is fathomable that inflammatory infiltrates triggered by SARS-CoV-2 infection may contribute to SSC development in our patient.…”

Section: Inflammation-mediated Sscmentioning

confidence: 70%

Secondary sclerosing cholangitis as a complication of severe COVID‐19: A case report and review of the literature

Klindt

Jensen

Brandenburger

et al. 2021

Clinical Case Reports

View full text Add to dashboard Cite

show abstract

Section: Inflammation-mediated Sscmentioning

confidence: 70%

Secondary sclerosing cholangitis as a complication of severe COVID‐19: A case report and review of the literature

Klindt

Jensen

Brandenburger

et al. 2021

Clinical Case Reports

View full text Add to dashboard Cite

show abstract

“…Again our data need to be interpreted with caution, since our findings cannot dismiss a role for TNFR 2 -mediated pathways or alternative activation in DDC-fed TNFR 1 −/− mice. In addition, signalling via alternative TNF receptors was sufficient to induced cholangitis in chronic Cyryptosporidium parvum -infected mice in single TNFR knock-out mice 51 . Alternative strategies to overcome inherent problems of these systems could lay in the generation of conditional knock-out mice.…”

Section: Discussionmentioning

confidence: 96%

The role of osteopontin and tumor necrosis factor alpha receptor-1 in xenobiotic-induced cholangitis and biliary fibrosis in mice

Fickert

Thueringer

Moustafa

et al. 2010

Laboratory Investigation

View full text Add to dashboard Cite

Background & Aims Proinflammatory and profibrotic cytokines such as osteopontin (OPN) and tumor necrosis factor-alpha receptor 1 (TNFR1) may be critically involved in the pathogenesis of cholangiopathies and biliary fibrosis. We therefore aimed to determine the role of genetic loss of either OPN or TNFR1 in 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-fed mice as a model of xenobiotic-induced sclerosing cholangitis with biliary-type liver fibrosis using respective knock-out mice. Methods OPN and TNFR1 knock-out mice were fed a 0.1% DDC-supplemented diet for 4 weeks and compared to corresponding wild type (WT) controls. Liver morphology (H&E staining), serum markers of liver injury and cholestasis (ALT, AP, bilirubin), markers of inflammation in liver (CD11b and F4/80 immunostaining, mRNA expression of iNOS, MCP-1, IL-1β, INF-γ, TNF-α, and OPN), degree of ductular reaction (immunohistochemistry with morphometric analysis and Western blotting for cholangiocyte specific marker keratin 19) and degree of liver fibrosis (Sirius red-staining, hepatic hydroxyproline content for quantification) were compared between groups. Results DDC feeding in OPN and TNFR1 knock-out mice and respective WT controls resulted in comparable extent of liver injury, inflammatory response, ductular reaction, and liver fibrosis. Summary & Conclusions Our data indicate that genetic loss of neither OPN nor TNFR1 significantly impacts on the pathogenesis of DDC-induced sclerosing cholangitis, ductular reaction and resulting biliary fibrosis.

show abstract

“…64 In mouse knockout models of secondary sclerosing cholangitis, production of TNFa in the bile ducts and signaling through TNF receptors (Tnfrsf1a/1b or Tnfrsf5) were obligatory for development of cholangitis. 65…”

Section: Mhc Genes and Susceptibility To Pscmentioning

confidence: 99%

Etiopathogenesis of Primary Sclerosing Cholangitis

2006

View full text Add to dashboard Cite

The etiopathogenesis of primary sclerosing cholangitis (PSC) remains undefined. Immunopathogenetic mechanisms appear to be involved, based on human leukocyte antigen complex susceptibility associations, existence of multiple autoantibodies, and presence of inflammatory bowel disease in > 75% of patients. PSC may represent an autoimmune disease with atypical features or an immune-mediated inflammatory disease, similar to inflammatory bowel disease itself. Immunogenetic susceptibility is closely linked to ligands for innate immune cells and capacity for sustained production of proinflammatory cytokines. Immunopathogenesis involves a multistep process initiated by the activation of cholangiocyte by bacterial pathogen-associated molecular patterns (stimuli of innate immunity) and proinflammatory cytokines in conjunction with aberrant expression of gut-specific chemokines and endothelial cell adhesion molecules in the liver. After recruitment of gut-primed memory T cells into the portal tracts and peribiliary space, additional mechanisms produce focal, fibrous, obliterative lesions. Progressive periductal fibrosis, chronic inflammation, and ischemic atrophy of biliary epithelia result in ductopenia, cholestasis, and obstructive strictures, culminating in secondary biliary cirrhosis.

show abstract

Requirement for TNF-Tnfrsf1 signalling for sclerosing cholangitis in mice chronically infected byCryptosporidium parvum

Cited by 20 publications

References 16 publications

Secondary sclerosing cholangitis as a complication of severe COVID‐19: A case report and review of the literature

Secondary sclerosing cholangitis as a complication of severe COVID‐19: A case report and review of the literature

The role of osteopontin and tumor necrosis factor alpha receptor-1 in xenobiotic-induced cholangitis and biliary fibrosis in mice

Etiopathogenesis of Primary Sclerosing Cholangitis

Contact Info

Product

Resources

About