Serum IL-33 Levels Are Associated with Liver Damage in Patients with Chronic Hepatitis B

Wang, Juan; Cai, Yong; Ji, Huifan; Feng, Junyan; Ayana, Desalegn Admassu; Niu, Junqi; Jiang, Yanfang

doi:10.1089/jir.2011.0109

Cited by 59 publications

(45 citation statements)

References 30 publications

(6 reference statements)

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“…Results of IHC staining for IL‐33 were similar to the findings of previous reports . IL‐33 staining was concentrated in the nuclei of vascular endothelial cells and sinusoidal endothelial cells in areas of inflammation.…”

Section: Discussionsupporting

confidence: 87%

“…IL‐33 has been reported to correlate with liver injury in patients with primary biliary cirrhosis (PBC) . Notably, serum levels of IL‐33 were closely associated with the degree of liver injury in patients with hepatitis B virus (HBV) infection . Moreover, the evaluation of dynamic changes in sST2 levels in HBV acute‐on‐chronic liver failure showed that serum sST2 levels increased over time in patients who died during follow‐up but decreased in those who survived.…”

mentioning

confidence: 99%

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Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Abe¹,

Takahashi²,

Fujita³

et al. 2019

Hepatol Commun

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Interleukin (IL)‐33 was recently described as a new member of the IL‐1 family; members of this family have proinflammatory activity. IL‐33 and its soluble receptor ST2 (sST2) have been implicated in the pathogenesis of autoimmune diseases. This study investigated serum IL‐33 and sST2 in type I autoimmune hepatitis (AIH) and the relationship of these molecules with clinical and pathologic parameters. Subjects included 65 patients with AIH who were diagnosed in our hospital. The control population included 17 healthy individuals and 36 patients with primary biliary cholangitis (PBC). Mean age at AIH diagnosis was 55.5 years, and the male‐to‐female ratio was 6:59. Serum IL‐33 and sST2 levels were significantly higher in patients with AIH than in those with PBC or controls. Importantly, immunohistochemistry revealed high IL‐33 expression in liver sections from patients with AIH. In particular, serum IL‐33 and sST2 levels were significantly higher in acute‐onset AIH than in chronic‐onset AIH. Serum IL‐33 levels were positively correlated with serum total bilirubin (TB), alanine aminotransferase (ALT), and necroinflammatory activity in AIH. We performed multivariate logistic regression analysis and found serum IL‐33 levels to be independent factors for severe activity. Serum sST2 levels were positively correlated with serum TB and ALT and negatively correlated with serum albumin and prothrombin time in AIH. In particular, serum sST2 levels were significantly higher in severe symptoms of AIH. Serum IL‐33 and sST2 levels in patients with AIH responsive to treatment with prednisolone were significantly decreased after treatment. Interestingly, serum IL‐33 level was associated with a significantly increased risk of relapse. Conclusion: IL‐33/ST2 may play an important role in the pathogenesis and severity of AIH and may be a promising target for AIH therapy.

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Section: Discussionsupporting

confidence: 87%

mentioning

confidence: 99%

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Abe¹,

Takahashi²,

Fujita³

et al. 2019

Hepatol Commun

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“…Such an understanding is supported by the markedly elevated serum levels of TGF-␤1 and IL-31 in ACLF patients and by the strong correlation between them in our study. Furthermore, we also found the serum levels of IL-17, IL-22, IL-33, and IL-35 were significantly increased in ACLF patients compared to the NC group, and serum levels of TGF-␤1 and IL-31 were all positively correlated with IL-17, IL-22, and IL-33, which have all been demonstrated to be proinflammatory cytokines in HBV-related diseases (23,32,33). Also, we found that serum levels of IL-9, IL-10, and IL-35 were elevated in the nonsurvivor ACLF patients.…”

Section: Discussionmentioning

confidence: 54%

The Transforming Growth Factor β1/Interleukin-31 Pathway Is Upregulated in Patients with Hepatitis B Virus-Related Acute-on-Chronic Liver Failure and Is Associated with Disease Severity and Survival

Guo

Ming

et al. 2015

Clin. Vaccine Immunol.

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The transforming growth factor ␤1/interleukin-31 (TGF-␤1/IL-31) pathway plays an important role in the process of cell injury and inflammation. The purpose of this work was to explore the role of the TGF-␤1/IL-31 pathway in the cytopathic process of hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF). The quantitative serum levels of TGF-␤1, IL-9, IL-10, IL-17, IL-22, IL-23, IL-31, IL-33, and IL-35 were analyzed among chronic hepatitis B (CHB) patients (n ‫؍‬ 17), ACLF patients (n ‫؍‬ 18), and normal control (NC) subjects (n ‫؍‬ 18). Disease severity in patients with ACLF was assessed using the model for endstage liver disease (MELD) and Child-Pugh scores. Serum TGF-␤1 levels were strongly positively correlated with IL-31 in all subjects, and both of them were positively correlated with IL-17, IL-22, and IL-33. In CHB and ACLF patients, serum levels of TGF-␤1 and IL-31 were both increased significantly compared with those in NC subjects and positively correlated with total bilirubin (TBil) and alpha-fetoprotein (AFP) levels. ACLF patients showed the highest levels of TGF-␤1 and IL-31, which were positively correlated with Child-Pugh scores. Furthermore, the recovery from the liver injury in CHB was accompanied by decreased TGF-␤1 and IL-31 levels. More importantly, serum levels of TGF-␤1 and IL-31 were markedly upregulated in ACLF nonsurvivors, and IL-31 displayed the highest sensitivity and specificity (85.7% and 100.0%, respectively) in predicting nonsurvival of ACLF patients. Increasing activity of the TGF-␤1/IL-31 pathway is well correlated with the extent of liver injury, disease severity, and nonsurvival of ACLF patients, while reducing activity is detected along the recovery from liver injury in CHB, suggesting its potential role in the pathogenesis of liver injury during chronic HBV infection. Hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF) is triggered mainly by severe extensive liver injury, and the exact mechanisms of massive destruction of HBV-infected hepatocytes remain unclear. However, one of the current assumptions is that the imbalance of the cytokine network, the so-called cytokine storm theory (1), points to potential involvement of inflammatory cytokines in destroying the HBV-infected cells, which may provide an explanation for the aggravation of liver injury.Transforming growth factor-␤1 (TGF-␤1) is a 25-kDa homodimeric protein composed of two subunits linked by a disulfide bond and is a powerful inhibitor of DNA synthesis and cellular proliferation (2). It also mediates formation of extracellular matrix and facilitates cell differentiation (3). Previous studies have shown that TGF-␤1 plays a role in developing liver failure (LF). Miwa et al. found that the mRNA and protein expression of TGF-␤1 were significantly upregulated in both the plasma and liver tissue in patients with fulminant liver failure (FLF) (4). Yoshimoto et al. found that the overexpression of TGF-␤1 delayed liver regeneration and promoted perisinusoidal fibrosis and hepatocyte apoptos...

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“…In patients with chronic hepatitis B, the serum level of IL-33 was significantly higher than in healthy people. The level of cytokine decreased in serum in response to a 12-week treatment with adefovir dipivoxil (41). During hepatitis C, the serum level of IL-33 correlated with transaminase levels and was higher in patients with chronic hepatitis than in patients who spontaneously recovered or in healthy people (42).…”

Section: The Il-33/st2 Pathway and Viral Infectionsmentioning

confidence: 96%

Crucial and Diverse Role of the Interleukin-33/ST2 Axis in Infectious Diseases

et al. 2015

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Serum IL-33 Levels Are Associated with Liver Damage in Patients with Chronic Hepatitis B

Cited by 59 publications

References 30 publications

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

The Transforming Growth Factor β1/Interleukin-31 Pathway Is Upregulated in Patients with Hepatitis B Virus-Related Acute-on-Chronic Liver Failure and Is Associated with Disease Severity and Survival

Crucial and Diverse Role of the Interleukin-33/ST2 Axis in Infectious Diseases

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