Expression of AIM2 is correlated with increased inflammation in chronic hepatitis B patients.
Virol J
; 12: 129, 2015 Aug 20.
Article
em En
| MEDLINE
| ID: mdl-26290184
BACKGROUND: The absent in melanoma 2 (AIM2), a cytosolic dsDNA inflammasome, can be activated by viral DNA to trigger caspase-1. Its role in immunopathology of chronic hepatitis B and C virus (HBV, HCV) infection is still largely unclear. In this study, the expression AIM2, and its downstream cytokines, caspase-1, IL-18 and IL-1ß, in liver tissue of patients with chronic hepatitis B and C (CHB, CHC) were investigated. METHODS: A total of 70 patients diagnosed with chronic hepatitis were enrolled, including 47 patients with CHB and 23 patients with CHC. A liver biopsy was taken from each patient, and immunohistochemistry was used to detect the expression of AIM2 and inflammatory factors caspase-1, IL-18, and IL-1ß in the biopsy specimens. The relationship between AIM2 expression and these inflammatory factors was analyzed. RESULTS: The expression of AIM2 in CHB patients (89.4 %) was significantly higher than in CHC patients (8.7 %), and among the CHB patients, the expression of AIM2 was significantly higher in the high HBV replication group (HBV DNA ≥ 1 × 10(5)copies/mL) than in the low HBV replication group (HBV DNA < 1 × 10(5)copies/mL). The expression of AIM2 was also correlated with HBV-associated inflammatory activity in CHB patients statistically. Additionally, AIM2 levels were positively correlated with the expression of caspase-1, IL-1ß and IL-18 in CHB patients, which implied that the AIM2 expression is directly correlated with the inflammatory activity associated with CHB. CONCLUSIONS: AIM2 upregulation may be a component of HBV immunopathology. The underlying mechanism and possible signal pathway warrant further study.
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Base de dados:
MEDLINE
Assunto principal:
Hepatite B Crônica
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Hepatite C Crônica
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Perfilação da Expressão Gênica
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Proteínas de Ligação a DNA
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Inflamação
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Fígado
Limite:
Adolescent
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Adult
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article