Publication: Hepatic macrophage activation and the LPS pathway
in patients with different degrees of severity and
histopathological patterns of drug induced liver injury
Authors
Du, Hui-juan ; Zhao, Su-xian ; Zhao, Wen ; Fu, Na ; Li, Wen-cong ; Qin, Xiao-jie ; Zhang, Yu-guo ; Nan, Yue-min ; Zhao, Jing-min
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-340
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info:eu-repo/semantics/article
Description
Abstract
Background. Inflammatory activation of
hepatic macrophages plays a primary role in druginduced liver injury (DILI). However, the exact
mechanism underlying DILI remains unclear.
Methods. A total of 328 DILI patients and 80 healthy
individuals were prospectively enrolled in this study.
The DILI patients were categorized into subgroups
based on either disease severity or histopathological
patterns. Plasma soluble CD163 (sCD163) and hepatic
CD163 were examined to determine hepatic macrophage
activation, and CD8, CD20, and MUM-1 were assessed
to determine cellular immunity using immunohistochemistry. The lipopolysaccharide (LPS) pathway
proteins [e.g. LPS, soluble CD14 (sCD14), and LPSbinding protein (LBP)] were measured using enzymelinked immunosorbent assay.
Results. Plasma sCD163 levels were nine-fold
higher in DILI patients than in healthy controls at the
baseline, but significantly decreased at the 4-week
follow-up visit after treatment. The numbers of hepatic
macrophages, B cells, and plasma cells were
significantly higher in the liver tissues from DILI
patients than those from healthy controls. Furthermore,
the baseline levels of LPS pathway proteins in the DILI
patients were significantly higher than those in the
controls. Notably, these proteins significantly decreased
at the 4-week follow-up visit but remained significantly
higher than the levels for the controls.
Conclusions. Hepatic inflammation in DILI involves
the activation of hepatic macrophages and cellular
immunity, in which the LPS pathway likely plays a role,
at least in part. As such, this study has improved our
understanding of the pathological mechanisms for DILI
and may facilitate the development of better treatments
for patients with DILI.
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