Cytokine production in patients with cirrhosis and TLR4 polymorphisms

World J Gastroenterol. 2014 Dec 14;20(46):17516-24. doi: 10.3748/wjg.v20.i46.17516.

Abstract

Aim: To analyze the cytokine production by peripheral blood cells from cirrhotic patients with and without TLR4 D299G and/or T399I polymorphisms.

Methods: The study included nine patients with cirrhosis and TLR4 D299G and/or T399I polymorphisms, and 10 wild-type patients matched for age, sex and degree of liver failure. TLR4 polymorphisms were determined by sequence-based genotyping. Cytokine production by peripheral blood cells was assessed spontaneously and also after lipopolysaccharide (LPS) and lipoteichoic acid (LTA) stimulation.

Results: Patients with TLR4 polymorphisms had a higher incidence of previous hepatic encephalopathy than wild-type patients (78% vs 20%, P = 0.02). Spontaneous production of interleukin (IL)-6 and IL-10 was lower in patients with TLR4 polymorphisms than in wild-type patients [IL-6: 888.7 (172.0-2119.3) pg/mL vs 5540.4 (1159.2-26053.9) pg/mL, P < 0.001; IL-10: 28.7 (6.5-177.1) pg/mL vs 117.8 (6.5-318.1) pg/mL, P = 0.02]. However, the production of tumor necrosis factor-α, IL-6 and IL-10 after LPS and LTA stimulation was similar in the two groups.

Conclusion: TLR4 polymorphisms were associated with a distinctive pattern of cytokine production in cirrhotic patients, suggesting that they play a role in the development of cirrhosis complications.

Keywords: Genetic factors; Hepatic encephalopathy; Infections; Inflammatory response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Case-Control Studies
  • Cells, Cultured
  • Cytokines / immunology
  • Cytokines / metabolism*
  • Disease Progression
  • Female
  • Genetic Association Studies
  • Genetic Predisposition to Disease
  • Hepatic Encephalopathy / genetics
  • Hepatic Encephalopathy / immunology
  • Hepatic Encephalopathy / metabolism
  • Humans
  • Interleukin-10 / metabolism
  • Interleukin-6 / metabolism
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / metabolism*
  • Lipopolysaccharides / pharmacology
  • Liver Cirrhosis / genetics*
  • Liver Cirrhosis / immunology
  • Liver Cirrhosis / metabolism
  • Male
  • Middle Aged
  • Phenotype
  • Polymorphism, Genetic*
  • Teichoic Acids / pharmacology
  • Toll-Like Receptor 4 / genetics*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • IL10 protein, human
  • IL6 protein, human
  • Interleukin-6
  • Lipopolysaccharides
  • TLR4 protein, human
  • Teichoic Acids
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • lipoteichoic acid