title: Dysfunction of splenic macrophages in cirrhotic patients with hypersplenism and HBV infection.
abstract: BACKGROUND
  Hepatitis B virus (HBV) reinfection is a difficult problem to manage after liver transplantation in patients with cirrhosis. This study was designed to investigate the activation type of splenic macrophages in cirrhotic patients with hypersplenism and HBV infection to assess the immune function of splenic macrophages.
  
  
  METHODS
  Fourteen cirrhotic patients with hypersplenism and HBV infection and 6 controls were enrolled in the study. Serum lipopolysaccharide (LPS) was detected with a limulus assay. The differential expression of cytokines by splenic tissue and splenic macrophages between the cirrhosis and control groups was compared with cytokine arrays. Furthermore, splenic macrophages were cultured and stimulated with LPS, after which tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 levels in the supernatant were determined.
  
  
  RESULTS
  In cirrhotic patients, serum LPS levels increased significantly. Interferon-gamma, TNF-beta, and transforming growth factor-beta upregulated, whereas IL-4 and IL-13 levels did not change in splenic tissue. TNF-alpha upregulated significantly, whereas IL-4 and IL-5 levels had no significant changes in splenic macrophages. The IL-12 levels in culture media of splenic macrophages from cirrhotic patients were significantly lower than in controls after LPS stimulation.
  
  
  CONCLUSIONS
  Splenic macrophages may be activated via incomplete M1 activation in cirrhotic patients with hypersplenism and HBV infection, and the immune function of splenic macrophages is impaired.
authors.affiliation: Department of General Surgery, The Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710004, China. aimin.li@yahoo.com
authors.forename: Aimin
authors.initials: A
authors.lastname: Li
authors.forename: Zongfang
authors.initials: Z
authors.lastname: Li
authors.forename: Shuangyu
authors.initials: S
authors.lastname: Ma
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Su
authors.forename: Shu
authors.initials: S
authors.lastname: Zhang
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Sun
authors.forename: Guowei
authors.initials: G
authors.lastname: Li
mesh_terms: D003470:Culture Media; D005355:Fibrosis / Q000150:complications / Q000276:immunology*; D006509:Hepatitis B / Q000150:complications / Q000276:immunology*; D006801:Humans; D018664:Interleukin-12 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000097:blood; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology*; D013154:Spleen / Q000276:immunology / Q000473:pathology*; D013163:Splenomegaly / Q000150:complications / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D003470:Culture Media; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12