The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Pathological bacterial translocation in liver cirrhosis
Open accessAbstract
Humans harbor nearly 100 trillion intestinal bacteria, which in terms of numbers, represents around ten times more microbial cells than eukaryotic cells. The gastrointestinal (GI) tract, the largest surface area of the body with an epithelial surface of approximately 400 m, is in constant exposure to these live microorganisms. Their peaceful coexistence demonstrated by the lack of pro-inflammatory responses against commensal bacteria implicates the presence of clearly defined lines of communication. In fact, bacterial translocation (BT), being defined as translocation of bacteria and/or bacterial products (lipopolysaccharides, peptidoglycans, muramyl-dipeptides, bacterial DNA, etc.) from the gut to mesenteric lymph nodes (MLN) [1], is a physiological process in healthy conditions and crucial for host immunity. In contrast, in cirrhosis ‘‘pathological’’ BT develops with a sustained increase in quantity (rate and/or degree) of BT. However, at least in humans, lack of access to MLN and/or upstream compartments towards the mucosal barrier until now hamper establishment of ‘‘cut-off’’ levels for physiological levels of BT in individual patients. Nonetheless, there appears to exist a hierarchy of three barriers against pathological BT, each of which encompasses a distinct set of mechanisms (Fig. 1). First, there are mediators that limit direct contact between the intestinal bacteria and the epithelial cell surface. Secondly, a layer of immune protection involves the rapid detection and killing of bacteria that manage to penetrate. Finally, a set of immune responses minimizes exposure of bacteria to the systemic immune system. In advanced liver cirrhosis, at each of these
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Cites
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“Abbreviations: AMP, antimicrobial peptides; APC, antigen-presenting cell; BDL, bile duct ligation; BT, bacterial translocation; CCl4, carbon-tetrachloride; DC, dendritic cell; FxR, Farnesoid X receptor; GALT, gut-associated lymphoid tissue; GI, gastrointestinal; GNB, gram-negative bacteria; HE, hepatic encephalopathy;…”
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Self-citation
Cited by
The gut-liver axis in liver disease: Pathophysiological basis for therapy
Albillos, A., de Gottardi, A., & Rescigno, M. (2020) · Journal of Hepatology · doi:10.1016/j.jhep.2019.10.003 · Cited by 2,166
Drug-Resistant E. coli Bacteremia Transmitted by Fecal Microbiota Transplant
DeFilipp, Z., Bloom, P. P., Torres Soto, M., Mansour, M. K., Sater, M. R. A., Huntley, M. H., Turbett, S., Chung, R. T., Chen, Y.-B., & Hohmann, E. L. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1910437 · Cited by 1,281
Cirrhosis-associated immune dysfunction: Distinctive features and clinical relevance
Albillos, A., Lario, M., & Álvarez-Mon, M. (2014) · Journal of Hepatology · doi:10.1016/j.jhep.2014.08.010 · Cited by 1,242
Interactions Between the Intestinal Microbiome and Liver Diseases
Schnabl, B., & Brenner, D. A. (2014) · Gastroenterology · doi:10.1053/j.gastro.2014.01.020 · Cited by 971
Gut–Liver Axis in Alcoholic Liver Disease
Szabo, G. (2015) · Gastroenterology · doi:10.1053/j.gastro.2014.10.042 · Cited by 754
Metadata
- Authors
- Wiest, R., Lawson, M., & Geuking, M.
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 60
- Issue
- 1
- Pages
- 197-209
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W2093795546
- Cited by
- 805
- References
- 29
- FWCI
- 23.31
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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