Chronic liver fibrosis induction in aging causes significant ultra-structural deterioration in liver and alteration on immune response gene expressions in liver-spleen axis.

IF 1.1 4区医学 Q4 MICROSCOPY

Ultrastructural Pathology Pub Date : 2024-07-03 Epub Date: 2024-06-06 DOI:10.1080/01913123.2024.2360447

Zeynal Mete Karaca, Gamze Karaca, Başak Kayhan, Mehmet Gül, Veysel Ersan, Harika Gözükara Bağ, Elif Yeşilada

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Abstract

The relationship between damage to the liver and spleen by aging and the immune response status in these two organs, which are anatomically and immunologically interconnected, is unknown. The authors investigated the histopathological, ultrastructural, and immunological effects of aging in young and aged fibrotic mice by using an experimental model. Four groups were planned, with 10 mice in each experimental group. The levels of fibrosis and ultrastructural destruction in the liver were determined by α-SMA staining and TEM analysis. Expression levels of immunity genes (Il2, Il4, Il6, Il10, Il12, Il17, Tnf, Ifng, Tgfb1, Gata3, Rorc, Tbx21, Foxp3, Ccl2, Ccr2, Cxcr3, Pf4, Cxcl10) were carried out by qRT-PCR. While structural disorders were detected in the mitochondria of aged healthy group, cellular destruction in the fibrosis-induced elderly group was at a dramatic level. Fibrosis induction in aged mice caused an elevation in the expression of chemokines (CCl2, CXCL10, CCR2) and cytokine (IL-17a) genes that induce autoinflammatory response in the liver. Unlike the cellular pathology and genes activated in fibrosis in youth and the natural occurrence of fibrosis with aging, induction of fibrosis during aging causes deterioration in the liver and expression of genes responsible for autoimmunity in both the liver and spleen.

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衰老诱导的慢性肝纤维化会导致肝脏超结构显著恶化，并改变肝脾轴心的免疫反应基因表达。

肝脏和脾脏在解剖学和免疫学上相互关联，而衰老对肝脏和脾脏的损伤与这两个器官的免疫反应状态之间的关系尚不清楚。作者通过实验模型研究了衰老对年轻和老年纤维化小鼠的组织病理学、超微结构和免疫学影响。实验计划分为四组，每组 10 只小鼠。通过α-SMA染色和TEM分析确定肝脏纤维化和超微结构破坏的程度。免疫基因（Il2、Il4、Il6、Il10、Il12、Il17、Tnf、Ifng、Tgfb1、Gata3、Rorc、Tbx21、Foxp3、Ccl2、Ccr2、Cxcr3、Pf4、Cxcl10）的表达水平通过 qRT-PCR 进行检测。虽然在健康老年组的线粒体中检测到了结构紊乱，但在纤维化诱导的老年组中，细胞破坏却达到了惊人的程度。诱导老年小鼠纤维化会导致趋化因子（CCl2、CXCL10、CCR2）和细胞因子（IL-17a）基因的表达升高，从而诱发肝脏的自身炎症反应。与年轻时纤维化的细胞病理学和激活的基因以及随着年龄增长而自然发生的纤维化不同，衰老过程中纤维化的诱导会导致肝脏恶化以及肝脏和脾脏中负责自身免疫的基因的表达。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Ultrastructural Pathology 医学-病理学

CiteScore

2.00

自引率

10.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Ultrastructural Pathology is the official journal of the Society for Ultrastructural Pathology. Published bimonthly, we are the only journal to be devoted entirely to diagnostic ultrastructural pathology. Ultrastructural Pathology is the ideal journal to publish high-quality research on the following topics: Advances in the uses of electron microscopic and immunohistochemical techniques Correlations of ultrastructural data with light microscopy, histochemistry, immunohistochemistry, biochemistry, cell and tissue culturing, and electron probe analysis Important new, investigative, clinical, and diagnostic EM methods.