The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation

<p>Abstract</p> <p>Background</p> <p>The development of ascites in cirrhotic patients generally heralds a deterioration in their clinical status. A differential gene expression profile between alcohol- and hepatitis C virus (HCV)-related cirrhosis has been described fro...

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Main Authors: Tapia-Abellán Ana, Martínez-Esparza María, Ruiz-Alcaraz Antonio J, Hernández-Caselles Trinidad, Martínez-Pascual Cristina, Miras-López Manuel, Such José, Francés Rubén, García-Peñarrubia Pilar
Format: Article
Language:English
Published: BMC 2012-08-01
Series:BMC Immunology
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Online Access:http://www.biomedcentral.com/1471-2172/13/42
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author Tapia-Abellán Ana
Martínez-Esparza María
Ruiz-Alcaraz Antonio J
Hernández-Caselles Trinidad
Martínez-Pascual Cristina
Miras-López Manuel
Such José
Francés Rubén
García-Peñarrubia Pilar
author_facet Tapia-Abellán Ana
Martínez-Esparza María
Ruiz-Alcaraz Antonio J
Hernández-Caselles Trinidad
Martínez-Pascual Cristina
Miras-López Manuel
Such José
Francés Rubén
García-Peñarrubia Pilar
author_sort Tapia-Abellán Ana
collection DOAJ
description <p>Abstract</p> <p>Background</p> <p>The development of ascites in cirrhotic patients generally heralds a deterioration in their clinical status. A differential gene expression profile between alcohol- and hepatitis C virus (HCV)-related cirrhosis has been described from liver biopsies, especially those associated with innate immune responses. The aim of this work was to identify functional differences in the inflammatory profile of monocyte-derived macrophages from ascites in cirrhotic patients of different etiologies in an attempt to extrapolate studies from liver biopsies to immune cells in ascites. To this end 45 patients with cirrhosis and non-infected ascites, distributed according to disease etiology, HCV (n = 15) or alcohol (n = 30) were studied. Cytokines and the cell content in ascites were assessed by ELISA and flow cytometry, respectively. Cytokines and ERK phosphorylation in peritoneal monocyte-derived macrophages isolated and stimulated <it>in vitro</it> were also determined.</p> <p>Results</p> <p>A different pattern of leukocyte migration to the peritoneal cavity and differences in the primed status of macrophages in cirrhosis were observed depending on the viral or alcoholic etiology. Whereas no differences in peripheral blood cell subpopulations could be observed, T lymphocyte, monocyte and polymorphonuclear cell populations in ascites were more abundant in the HCV than the alcohol etiology. HCV-related cirrhosis etiology was associated with a decreased inflammatory profile in ascites compared with the alcoholic etiology<b>.</b> Higher levels of IL-10 and lower levels of IL-6 and IL-12 were observed in ascitic fluid from the HCV group. Isolated peritoneal monocyte-derived macrophages maintained their primed status <it>in vitro</it> throughout the 24 h culture period. The level of ERK1/2 phosphorylation was higher in ALC peritoneal macrophages at baseline than in HCV patients, although the addition of LPS induced a greater increase in ERK1/2 phosphorylation in HCV than in ALC patients.</p> <p>Conclusions</p> <p>The macrophage inflammatory status is higher in ascites of alcohol-related cirrhotic patients than in HCV-related patients, which could be related with differences in bacterial translocation episodes or regulatory T cell populations. These findings should contribute to identifying potential prognostic and/or therapeutic targets for chronic liver diseases of different etiology.</p>
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spelling doaj.art-ec98005cd89b49f291983030bfe6d82b2022-12-21T19:03:17ZengBMCBMC Immunology1471-21722012-08-011314210.1186/1471-2172-13-42The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylationTapia-Abellán AnaMartínez-Esparza MaríaRuiz-Alcaraz Antonio JHernández-Caselles TrinidadMartínez-Pascual CristinaMiras-López ManuelSuch JoséFrancés RubénGarcía-Peñarrubia Pilar<p>Abstract</p> <p>Background</p> <p>The development of ascites in cirrhotic patients generally heralds a deterioration in their clinical status. A differential gene expression profile between alcohol- and hepatitis C virus (HCV)-related cirrhosis has been described from liver biopsies, especially those associated with innate immune responses. The aim of this work was to identify functional differences in the inflammatory profile of monocyte-derived macrophages from ascites in cirrhotic patients of different etiologies in an attempt to extrapolate studies from liver biopsies to immune cells in ascites. To this end 45 patients with cirrhosis and non-infected ascites, distributed according to disease etiology, HCV (n = 15) or alcohol (n = 30) were studied. Cytokines and the cell content in ascites were assessed by ELISA and flow cytometry, respectively. Cytokines and ERK phosphorylation in peritoneal monocyte-derived macrophages isolated and stimulated <it>in vitro</it> were also determined.</p> <p>Results</p> <p>A different pattern of leukocyte migration to the peritoneal cavity and differences in the primed status of macrophages in cirrhosis were observed depending on the viral or alcoholic etiology. Whereas no differences in peripheral blood cell subpopulations could be observed, T lymphocyte, monocyte and polymorphonuclear cell populations in ascites were more abundant in the HCV than the alcohol etiology. HCV-related cirrhosis etiology was associated with a decreased inflammatory profile in ascites compared with the alcoholic etiology<b>.</b> Higher levels of IL-10 and lower levels of IL-6 and IL-12 were observed in ascitic fluid from the HCV group. Isolated peritoneal monocyte-derived macrophages maintained their primed status <it>in vitro</it> throughout the 24 h culture period. The level of ERK1/2 phosphorylation was higher in ALC peritoneal macrophages at baseline than in HCV patients, although the addition of LPS induced a greater increase in ERK1/2 phosphorylation in HCV than in ALC patients.</p> <p>Conclusions</p> <p>The macrophage inflammatory status is higher in ascites of alcohol-related cirrhotic patients than in HCV-related patients, which could be related with differences in bacterial translocation episodes or regulatory T cell populations. These findings should contribute to identifying potential prognostic and/or therapeutic targets for chronic liver diseases of different etiology.</p>http://www.biomedcentral.com/1471-2172/13/42AscitesCirrhosisCytokinesEtiologyMAP kinasesHCVAlcohol
spellingShingle Tapia-Abellán Ana
Martínez-Esparza María
Ruiz-Alcaraz Antonio J
Hernández-Caselles Trinidad
Martínez-Pascual Cristina
Miras-López Manuel
Such José
Francés Rubén
García-Peñarrubia Pilar
The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation
BMC Immunology
Ascites
Cirrhosis
Cytokines
Etiology
MAP kinases
HCV
Alcohol
title The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation
title_full The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation
title_fullStr The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation
title_full_unstemmed The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation
title_short The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation
title_sort peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis c viral etiology and is related to erk phosphorylation
topic Ascites
Cirrhosis
Cytokines
Etiology
MAP kinases
HCV
Alcohol
url http://www.biomedcentral.com/1471-2172/13/42
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