<i>NOD2</i> gene variants are a risk factor for culture‐positive spontaneous bacterial peritonitis and monomicrobial bacterascites in cirrhosis

Bruns, Tony; Peter, Jack; Reuken, Philipp; Grabe, Dominik H.; Schuldes, Sonja; Brenmoehl, Julia; Schölmerich, Jürgen; Wiest, Reiner; Stallmach, Andreas

doi:10.1111/j.1478-3231.2011.02561.x

Cited by 64 publications

(60 citation statements)

References 34 publications

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“…Of note, carriers of NOD2 risk alleles showed a significantly (p = 0.007) reduced mean survival time (274 days) in comparison to patients without mutations (395 days) [16] . This association was replicated for culture-positive SBP; an interesting finding in this study was that patients with NOD2 variants presented more often with variceal bleeding and hepatocellular carcinoma [17] .…”

Section: Liver Cirrhosissupporting

confidence: 60%

Genetics in Common Liver Diseases: From Pathophysiology to Precise Treatment

Lammert

2016

Dig Dis

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In the past 2 decades, advances in genetics have improved our understanding of liver disease and physiology. Firstly, developments in genomic technologies drove the identification of genes responsible for monogenic (Mendelian) liver diseases. Over the last decade, genome-wide association studies allowed for the dissection of the genetic susceptibility to complex liver diseases such as fatty liver disease and drug-induced liver injury, in which environmental co-factors play critical roles. The findings have allowed the identification and elaboration of pathophysiological processes, have indicated the need for reclassification of liver diseases and risk factors and have already pointed to new disease treatments. This is illustrated by the interaction of alcohol, overnutrition and the PNPLA3 gene, which represents an ‘infernal triangle' for the liver. In the future, genetics will allow further stratification of liver diseases and contribute to personalized (precision) medicine, offering novel opportunities for translational research and clinical care of our patients.

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Section: Liver Cirrhosissupporting

confidence: 60%

Genetics in Common Liver Diseases: From Pathophysiology to Precise Treatment

Lammert

2016

Dig Dis

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“…3 The expression of NF-jB was increased after 72 h stimulation by MDP and Af conidia; the effect was interrupted by RNA interference of NOD2. *p \ 0.05 versus control (CON), # p \ 0.05 versus without RNAi factors of bacterial infection and are associated with early mortality in sepsis patients [13,14]. Meanwhile, the effect of NOD2 in detecting microorganisms and induction of innate immune response was shown in Toxoplasma gondii [15], virals [16], Streptococcus pneumonia, Mycobacterium tuberculosis, Staphylococcus aureus [17,18], Listeria monocytogenes [19], and recently in the intracellular pathogens Legionella pneumophila [20] and Chlamydophila pneumonia [21].…”

Section: Discussionmentioning

confidence: 99%

Role of NOD2 in regulating the immune response to Aspergillus fumigatus

Tao

Zhang

et al. 2012

Inflamm. Res.

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“…In addition, essentially all animal models of intestinal fibrosis appear to be dependent on the presence of a microflora to initiate or perpetuate gut inflammation and fibrosis [25]. Although direct evidence about the innate immunity gene variants in liver fibrosis is lacking, several studies have shown that NOD2 is associated with the increased mortality in nonalcoholic liver transplant patients [30] or the increased risk of spontaneous bacterial peritonitis in patients with liver cirrhosis [31,32]. …”

Section: Innate Immunitymentioning

confidence: 99%

Intestinal Fibrosis and Liver Fibrosis: Consequences of Chronic Inflammation or Independent Pathophysiology?

Rieder¹,

Bettenworth²,

Imai³

et al. 2016

Inflamm Intest Dis

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Background: Intestinal fibrosis and liver fibrosis represent a significant burden for our patients and health-care systems. Despite the severe clinical problem and the observation that fibrosis is reversible, no specific antifibrotic therapies exist. Summary: In this review, using an ‘East-West' scientific collaboration, we summarize the current knowledge on principal mechanisms shared by intestinal fibrosis and liver fibrosis. We furthermore discuss inflammation as the cause of fibrogenesis in both entities, depict unique features of intestinal and hepatic fibrosis, and provide a future outlook on the development of antifibrotic therapies. Key Messages: A collaborative effort in the field of fibrosis, covering multiple organ systems, will have the highest chance of leading to the development of a successful antifibrotic intervention.

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NOD2 gene variants are a risk factor for culture‐positive spontaneous bacterial peritonitis and monomicrobial bacterascites in cirrhosis

Abstract: NOD2 variants increase the risk for culture-positive SBP and bacterascites in cirrhosis and may affect survival.

Cited by 64 publications

References 34 publications

Genetics in Common Liver Diseases: From Pathophysiology to Precise Treatment

Genetics in Common Liver Diseases: From Pathophysiology to Precise Treatment

Role of NOD2 in regulating the immune response to Aspergillus fumigatus

Intestinal Fibrosis and Liver Fibrosis: Consequences of Chronic Inflammation or Independent Pathophysiology?

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