Ascitic fluid regulates the local innate immune response of patients with cirrhosis
Por:
Nieto, JC, Perea, L, Soriano, G, Zamora, C, Canto, E, Medina, A, Poca, M, Sanchez, E, Roman, E, Julia, G, Navarro, F, Gely, C, Alvarado, EA, Guarner, C, Juarez, C, Vidal, S
Publicada:
1 oct 2018
Resumen:
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-1 beta, 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 oxidative burst 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-alpha 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-alpha 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.
Filiaciones:
Nieto, JC:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Perea, L:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Soriano, G:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Inst Salud Carlos III, CIBERehd, Madrid, Spain
Univ Autonoma Barcelona, Barcelona, Spain
Zamora, C:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Canto, E:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Medina, A:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Poca, M:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Inst Salud Carlos III, CIBERehd, Madrid, Spain
Sanchez, E:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Inst Salud Carlos III, CIBERehd, Madrid, Spain
Roman, E:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Inst Salud Carlos III, CIBERehd, Madrid, Spain
Univ Autonoma Barcelona, Barcelona, Spain
Escola Univ Infermeria EUI St Pau, Barcelona, Spain
Julia, G:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Navarro, F:
Hosp Santa Creu & Sant Pau, Dept Microbiol, Barcelona, Spain
Gely, C:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Alvarado, EA:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Guarner, C:
Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
Inst Salud Carlos III, CIBERehd, Madrid, Spain
Univ Autonoma Barcelona, Barcelona, Spain
Juarez, C:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Univ Autonoma Barcelona, Barcelona, Spain
Vidal, S:
Inst Recerca, Dept Immunol, Barcelona, Spain
Hosp Santa Creu & Sant Pau, Barcelona, Spain
Univ Autonoma Barcelona, Barcelona, Spain
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