慢性乙型肝炎肝硬化和非肝硬化患者炎症和凋亡生物特征的

StephenW

慢性乙型肝炎肝硬化和非肝硬化患者炎症和凋亡生物特征的比较表达
Muttiah Barathan 1，Behnaz Riazalhosseini 2，Thevambiga Iyadorai 3，Kumutha Malar Vellasamy 4，Jamuna Vadivelu 5，Li-Yen Chang 6，Ahmad Khusairy Zulpa 7，Marie Larsson 8，Esaki M Shankar 10
隶属关系
隶属关系

    1
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    2
    马来亚大学医学院药理学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    3
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    4
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    5
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址： [email protected]。
    6
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    7
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    8
    瑞典林雪平林雪平大学生物医学和临床科学系分子医学和病毒学部。电子地址：[email protected]。
    9
    马来亚大学医学院医学微生物学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。
    10
    马来亚大学医学院医学系，Lembah Pantai，吉隆坡，50603，马来西亚。电子地址：[email protected]。

    PMID：34619310 DOI：10.1016/j.micpath.2021.105231

抽象的

免疫介质的相互作用对于最佳宿主抗病毒免疫反应至关重要，尤其是针对慢性乙型肝炎病毒 (HBV) 感染。在这里，我们通过检查细胞凋亡的特征和促炎细胞因子、趋化因子和细胞毒性蛋白的血浆水平，研究了慢性 HBV 感染者有和没有肝硬化的宿主免疫反应的动态变化。研究了总共 40 名患有和不患有肝硬化的慢性 HBV 患者的免疫介质的血浆水平和外周血单核细胞 (PBMC) 的细胞凋亡特征。与慢性HBV患者相比，慢性HBV合并肝硬化患者的细胞内活性氧（ROS）浓度相对较高。由于持续的肝脏炎症与血浆 TNF-α 和 IL-6 水平一致，细胞凋亡的发生得以持续。血浆VEGF在慢性HBV肝硬化患者中上调，而CCL2、CCL5和颗粒酶B水平下调。高水平的 ROS、IL-6 和 TNF-α 与慢性 HBV 肝硬化患者的持续炎症相关，这可能归因于免疫细胞中细胞凋亡和活化的生物特征的表达。

关键词：细胞凋亡；趋化因子；细胞因子；炎; PBMC;等离子体。

版权所有 © 2021。由爱思唯尔有限公司出版。

StephenW

Comparative expression of inflammatory and apoptotic biosignatures in chronic-HBV patients with and without liver cirrhosis
Muttiah Barathan  1 , Behnaz Riazalhosseini  2 , Thevambiga Iyadorai  3 , Kumutha Malar Vellasamy  4 , Jamuna Vadivelu  5 , Li-Yen Chang  6 , Ahmad Khusairy Zulpa  7 , Marie Larsson  8 , Esaki M Shankar  9 , Rosmawati Mohamed  10
Affiliations
Affiliations

    1
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    2
    Department of Pharmacology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    3
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    4
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    5
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    6
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    7
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    8
    Division of Molecular Medicine and Virology, Department of Biomedicine and Clinical Sciences, Linköping University, Linköping, Sweden. Electronic address: [email protected].
    9
    Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].
    10
    Department of Medicine, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, 50603, Malaysia. Electronic address: [email protected].

    PMID: 34619310 DOI: 10.1016/j.micpath.2021.105231

Abstract

The interplay of immune mediators is paramount to optimal host anti-viral immune responses, especially against chronic hepatitis B virus (HBV) infection. Here, we investigated the dynamic changes in host immune responses in chronic HBV-infected individuals with and without liver cirrhosis by examining the signatures of apoptosis and plasma levels of pro-inflammatory cytokines, chemokines, and cytotoxic proteins. A total of 40 chronic HBV patients with and without liver cirrhosis were studied for plasma levels of immune mediators, and signatures of apoptosis in peripheral blood mononuclear cells (PBMCs). The intracellular concentrations of reactive oxygen species (ROS) in patients with chronic HBV with liver cirrhosis was relatively higher as compared to chronic HBV patients. The onset of apoptosis was sustained due to ongoing liver inflammation in concert with plasma TNF-α and IL-6 levels. Plasma VEGF was upregulated among chronic HBV patients with liver cirrhosis, whereas CCL2, CCL5 and granzyme B levels were down-regulated. High levels of ROS, IL-6 and TNF-α correlated with ongoing inflammation among chronic HBV patients with liver cirrhosis, which likely attributed to the expression of biosignatures of apoptosis and activation in immune cells.

Keywords: Apoptosis; Chemokine; Cytokine; Inflammation; PBMC; Plasma.

Copyright © 2021. Published by Elsevier Ltd.