Ascitic fluid regulates the local innate immune response of patients with cirrhosis

Ascitic neutrophils from cirrhotic patients with spontaneous bacterial peritonitis (SBP) exhibit an impaired oxidative burst that could facilitate bacterial infection. However, the influence of the cell-free ascitic fluid of these patients on neutrophil function has not been investigated. To analyze...

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Bibliographic Details
Authors: Nieto Sáchica, Juan Camilo|||0000-0002-3400-1488, Perea, Lidia|||0000-0002-1624-0012, Soriano, German|||0000-0002-9267-6811, Zamora, Carlos|||0000-0003-2962-678X, Cantó, Elisabet|||0000-0002-1782-1855, Medina Dols, Aina, Poca Pastor, María Antonia|||0000-0002-3831-0536, Sánchez, Elisabet|||0000-0002-3280-9301, Roman, Eva|||0000-0001-9084-8555, Julià, Germà, Navarro Risueño, Ferran|||0000-0002-4302-2838, Gely, Cristina|||0000-0003-0144-4650, Alvarado-Tapias, Edilmar|||0000-0003-2036-6133, Guarner-Argente, Carlos|||0000-0002-8180-1488, Juárez Rubio, Cándido|||0000-0003-2235-9893, Vidal, Silvia|||0000-0002-3909-6682
Format: article
Publication Date:2018
Country:España
Institution:Universitat Autònoma de Barcelona
Repository:Dipòsit Digital de Documents de la UAB
Language:English
OAI Identifier:oai:ddd.uab.cat:285284
Online Access:https://ddd.uab.cat/record/285284
https://dx.doi.org/urn:doi:10.1002/JLB.3A0218-072R
Access Level:Open access
Keyword:NETosis
Oxidative burst
Resistin
Spontaneous bacterial peritonitis
Description
Summary:Ascitic neutrophils from cirrhotic patients with spontaneous bacterial peritonitis (SBP) exhibit an impaired oxidative burst that could facilitate bacterial infection. However, the influence of the cell-free ascitic fluid of these patients on neutrophil function has not been investigated. To analyze this influence, we determined the ascitic levels of cytokines, resistin, and lactoferrin and their association with neutrophil function, disease severity score, and SBP resolution. We analyzed NETosis induction by microscopy and oxidative burst by the flow cytometry of healthy neutrophils cultured in ascitic fluid from cirrhotic patients with sterile ascites (SA) and with SBP before and after antibiotic treatment. Resistin, IL-6, IL-1 receptor antagonist, IL-1β, and lactoferrin levels were measured in ascitic fluids and supernatants of cultured neutrophils and PBMCs by ELISA. Upon stimulation, healthy neutrophils cultured in SBP ascitic fluid produced lower NETosis and oxidativeburst than those cultured in SA. Ascitic resistin levels were negatively correlated with NETosis, oxidative burst, and ascitic glucose levels; and positively correlated with the model for end-stage liver disease score. After an E. coli or TNF-α stimulus, neutrophils were the major resistin producers. Resistin indirectly reduced the oxidative burst of neutrophils and directly reduced the inflammatory phenotype of monocytes and TNF-α production. Bacterial-induced resistin production can down-regulate the inflammatory response of macrophages and neutrophil function in ascitic fluid. Consequently, this down-regulation may jeopardize the elimination of bacteria that translocate to ascitic fluid in patients with cirrhosis.

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