4.5 Article

Significant hepatic expression of IL-2 and IL-8 in biliary atresia compared with other neonatal cholestatic disorders

期刊

CYTOKINE
卷 79, 期 -, 页码 59-65

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ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2015.12.023

关键词

Biliary atresia; Interleukin 2; Interleukin 8; Etiopathogenesis; Immunostaining; Neonatal cholestasis

资金

  1. National Liver Institute

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Objectives: Although the exact etiology of biliary atresia (BA) is still elusive, inflammation plays a key role. Release of proinflammatory cytokines from activated immune cells perpetuates the injury and causes biliary destruction. We aimed to study interleukin (IL)-2 and IL-8 expression in liver tissue of BA patients compared with other neonatal cholestatic disorders. Methods: The study included 59 infants with neonatal cholestasis in two groups; BA group (n = 31) and non-BA group (n = 28) with cholestatic disorders other than BA as controls. Demographic, clinical, laboratory, and histopathological parameters were collected. IL-2 and IL-8 immunostaining was performed. Immunostaining in portal cellular infiltrate was scored as positive or negative and expressed as the mean cell count in three portal tracts. Results: The mean value of IL-2 and IL-8 positive inflammatory cells was significantly higher in BA than in non-BA group (P-values of 0.004 and 0.002 respectively). IL-2 correlated significantly with IL-8 immunostaining in both BA and non-BA group (P < 0.0001 for both). Furthermore, both cytokines in both groups correlated significantly with inflammatory activity in liver biopsy while there was no significant correlation with the other studied parameters. Yet, there was a trend of increased expression of IL-2 and IL-8 with increasing stage of fibrosis in BA group. This trend was not observed in non-BA group. Conclusion: The significantly higher expression of IL-2 and IL-8 in patients with BA compared to non-BA suggests a potential role for these cytokines in the pathogenesis in therapy of this devastating neonatal hepatic disorder. (C) 2015 Elsevier Ltd. All rights reserved.

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