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Systemic inflammation in absence of gut bacterial translocation in C57BL/6 mice with cirrhosis
  1. María Úbeda1,2,
  2. Margaret Lario1,2,
  3. Leticia Muñoz1,2,
  4. David Díaz1,2,
  5. María José Borrero1,2,
  6. Laura García-Bermejo3,
  7. Melchor Álvarez-Mon1,2,4,
  8. Agustín Albillos1,2,5
  1. 1Laboratory of Immune System Diseases, Department of Medicine, University of Alcalá, Alcalá de Henares, Madrid, Spain
  2. 2Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd), Instituto de Salud Carlos III, Madrid, Spain
  3. 3Department of Pathology, Hospital Universitario Ramón y Cajal, IRYCIS, Madrid, Spain
  4. 4Department of Immune System Diseases and Oncology, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
  5. 5Department of Gastroenterology, Hospital Universitario Ramón y Cajal, IRYCIS, Madrid, Spain
  1. Correspondence to Professor Agustín Albillos, Departamento de Medicina, Facultad de Medicina-Campus Universitario, Universidad de Alcalá, Carretera Madrid-Barcelona km. 33.600, Alcalá de Henares 28871, Madrid, Spain; aalbillosm{at}meditex.es

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We read with interest the article by Wiest et al about spontaneous bacterial peritonitis guidelines.1 The authors point out the relevance of pathological bacterial translocation (BT) from the gut to mesenteric lymph nodes (MLN) as the pathophysiological hallmark of spontaneous bacterial peritonitis in cirrhosis, and the need of further research in the factors involved in BT. The study of BT, ascites and related immune system abnormalities in carbon tetrachloride (CCl4) cirrhosis is usually conducted in rats. This model has proved useful for research into the pathogenesis and role of the systemic pro-inflammatory response associated with cirrhosis and its link to BT.2–4 We recently showed that modulation of the immune system response in cirrhotic rats …

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