Publication:
Is the development of ascites in alcoholic liver patients influenced by specific KIR/HLA Gene profiles?

dc.contributor.authorMorales, Raquel
dc.contributor.authorBolarín, José Miguel
dc.contributor.authorCollados Ros, Aurelia
dc.contributor.authorPons, José Antonio
dc.contributor.authorMuro, Manuel
dc.contributor.authorLegaz Pérez, Isabel
dc.contributor.departmentCiencias Sociosanitarias
dc.date.accessioned2024-07-08T11:34:03Z
dc.date.available2024-07-08T11:34:03Z
dc.date.issued2023-08-28
dc.description© 2023 by the authors. This manuscript version is made available under the CC-BY 4.0 license http://creativecommons.org/licenses/by/4.0/. This document is the Published version of a Published Work that appeared in final form in Biomedicines. To access the final edited and published work see https://doi.org/10.3390/biomedicines11092405
dc.description.abstractDecompensated cirrhosis is the most common cause of ascites due to hemodynamic and renal alteration by continuous fluid leakage from the hepatic sinusoids and splanchnic capillaries into the interstitial space. Then, fluid leakage exceeds lymphatic return, leading to progressive fluid accumulation directly into the peritoneal cavity. Alcohol consumption is one of the main risks of developing alcoholic cirrhosis (AC), but not all AC patients develop ascites. Avoiding the development of ascites is crucial, given that it deteriorates prognosis and increases the patient mortality patient. The innate immune system plays a crucial role in cirrhosis through natural killer cells, which are abundant in the liver. The aim of this study was to analyze the KIR/HLA-C genetic profile in AC patients with and without ascites to understand this pathology and find predictive clinical susceptibility biomarkers that can help to establish risks and prevent the development of ascites in AC patients. A total of 281 AC patients with and without ascites were analyzed and compared with 319 healthy controls. Genomic DNA was extracted from peripheral blood in all groups. A PCR-SSO assay was performed for KIR/HLA genotyping analysis. A total of 16 activating and inhibitor KIR genes and their corresponding known ligands, epitopes of HLA-C, and their genotypes were analyzed. According to our analysis, C1 epitopes were statistically significantly decreased in AC patients with and without ascites. When comparing AC patients with ascites and healthy controls, a significant decrease in C1 epitope frequency was also observed. A statistically significant decrease was also found when comparing the C1C2 genotype in AC patients without ascites with controls. In conclusion, the absence of KIR2DL2 and KIR3DL1 genes may be a predisposing factor for the development of ascites in AC patients. The KIR2DS2/KIR2DL2 may could be involved in grade I ascites development, and the presence of the C1+ epitope and the homozygous C2C2 genotype may be protective genetic factors against ascites development in AC patients.es
dc.formatapplication/pdfes
dc.format.extent18es
dc.identifier.citationBiomedicines 2023, 11(9), 2405
dc.identifier.doihttps://doi.org/10.3390/biomedicines11092405
dc.identifier.issnElectronic: 2227-9059
dc.identifier.urihttp://hdl.handle.net/10201/142910
dc.languageenges
dc.publisherMDPI
dc.relationOur work was possible thanks to support from Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy, and Competitiveness (grant number P19/01194) and co-funding from the European Union through the European Fund of Regional Development (FEDER) with the principle of “A manner to build Europe”.es
dc.relation.publisherversionhttps://www.mdpi.com/2227-9059/11/9/2405
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectAlcoholic cirrhosises
dc.subjectAsciteses
dc.subjectHuman clinical toxicologyes
dc.subjectLiver transplantes
dc.subjectKIR/HLA-C geneses
dc.titleIs the development of ascites in alcoholic liver patients influenced by specific KIR/HLA Gene profiles?es
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
relation.isAuthorOfPublicationb83b4b59-2d61-40f0-9108-5c6a6d158295
relation.isAuthorOfPublication.latestForDiscoveryb83b4b59-2d61-40f0-9108-5c6a6d158295
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