Th1/Th2 Cells and Associated Cytokines in Acute Hepatitis E and Related Acute Liver Failure
Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). Methods. We evaluated viral load and Th...
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Published in | Journal of Immunology Research Vol. 2020; no. 2020; pp. 1 - 8 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Cairo, Egypt
Hindawi Publishing Corporation
2020
Hindawi John Wiley & Sons, Inc Hindawi Limited |
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Abstract | Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). Methods. We evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. Results. There was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both P>0.05). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both P<0.05), but there was no significant difference between the AHE and HEV-ALF groups (P>0.05). Both IFN-γ and IL-10 showed gradual upward trend from the HC group to the AHE (both P<0.01), but IFN-γ showed a sharp downward trend from the AHE group to the HEV-ALF group (P<0.01) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group (P<0.01).There was no significant difference in Th1 and Th2 cytokines between the HEV RNA(+) group and HEV RNA(-) group (all P>0.05). Th2 bias was observed from the AHE (ratio=58.65) to HEV-ALF (ratio=1.20) groups. The level of IFN-γ was associated with the outcome of HEV-ALF patients. Conclusions. HEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE. |
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AbstractList | Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). Methods. We evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. Results. There was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both P>0.05). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both P0.05). Both IFN-γ and IL-10 showed gradual upward trend from the HC group to the AHE (both P<0.01), but IFN-γ showed a sharp downward trend from the AHE group to the HEV-ALF group (P<0.01) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group (P0.05). Th2 bias was observed from the AHE (ratio=58.65) to HEV-ALF (ratio=1.20) groups. The level of IFN-γ was associated with the outcome of HEV-ALF patients. Conclusions. HEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE. Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). Methods. We evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. Results. There was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both P > 0.05 ). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both P < 0.05 ), but there was no significant difference between the AHE and HEV-ALF groups ( P > 0.05 ). Both IFN-γ and IL-10 showed gradual upward trend from the HC group to the AHE (both P < 0.01 ), but IFN-γ showed a sharp downward trend from the AHE group to the HEV-ALF group ( P < 0.01 ) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group ( P < 0.01 ).There was no significant difference in Th1 and Th2 cytokines between the HEV RNA(+) group and HEV RNA(-) group (all P > 0.05 ). Th2 bias was observed from the AHE ( ratio = 58.65 ) to HEV-ALF ( ratio = 1.20 ) groups. The level of IFN-γ was associated with the outcome of HEV-ALF patients. Conclusions. HEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE. Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). Methods. We evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. Results. There was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both P>0.05). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both P<0.05), but there was no significant difference between the AHE and HEV-ALF groups (P>0.05). Both IFN-γ and IL-10 showed gradual upward trend from the HC group to the AHE (both P<0.01), but IFN-γ showed a sharp downward trend from the AHE group to the HEV-ALF group (P<0.01) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group (P<0.01).There was no significant difference in Th1 and Th2 cytokines between the HEV RNA(+) group and HEV RNA(-) group (all P>0.05). Th2 bias was observed from the AHE (ratio=58.65) to HEV-ALF (ratio=1.20) groups. The level of IFN-γ was associated with the outcome of HEV-ALF patients. Conclusions. HEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE. BACKGROUND AND AIMSThe involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). METHODSWe evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. RESULTSThere was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both P > 0.05). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both P < 0.05), but there was no significant difference between the AHE and HEV-ALF groups (P > 0.05). Both IFN-γ and IL-10 showed gradual upward trend from the HC group to the AHE (both P < 0.01), but IFN-γ showed a sharp downward trend from the AHE group to the HEV-ALF group (P < 0.01) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group (P < 0.01).There was no significant difference in Th1 and Th2 cytokines between the HEV RNA(+) group and HEV RNA(-) group (all P > 0.05). Th2 bias was observed from the AHE (ratio = 58.65) to HEV-ALF (ratio = 1.20) groups. The level of IFN-γ was associated with the outcome of HEV-ALF patients. CONCLUSIONSHEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). We evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. There was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both > 0.05). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both < 0.05), but there was no significant difference between the AHE and HEV-ALF groups ( > 0.05). Both IFN- and IL-10 showed gradual upward trend from the HC group to the AHE (both < 0.01), but IFN- showed a sharp downward trend from the AHE group to the HEV-ALF group ( < 0.01) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group ( < 0.01).There was no significant difference in Th1 and Th2 cytokines between the HEV RNA(+) group and HEV RNA(-) group (all > 0.05). Th2 bias was observed from the AHE (ratio = 58.65) to HEV-ALF (ratio = 1.20) groups. The level of IFN- was associated with the outcome of HEV-ALF patients. HEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE. |
Audience | Academic |
Author | Huang, Fen Wu, Jian Wei, Daqiao Li, Lanjuan Guo, Yurong Jiang, Bin Lu, Xuan Shang, Anquan Lv, Feifei Pan, Qiaoling Yu, Jiong Yang, Jinfeng Cao, Hongcui |
AuthorAffiliation | 2 Department of Laboratory Medicine, Yancheng Clinical Medical College of Nanjing Medical University, Yancheng 224001, China 6 Department of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Shanghai 200065, China 5 Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China 8 Zhejiang Provincial Key Laboratory for Diagnosis and Treatment of Aging and Physic-chemical Injury Diseases, 79 Qingchun Rd, Hangzhou 310003, China 4 Medical School, Kunming University of Science and Technology, 727 Jing Ming South Road, Kunming 650031, China 1 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Rd., Hangzhou 310003, China 3 Department of Laboratory Medicine, Yancheng Hospital of Traditional Chinese Medicine, Affiliated to Nanji |
AuthorAffiliation_xml | – name: 3 Department of Laboratory Medicine, Yancheng Hospital of Traditional Chinese Medicine, Affiliated to Nanjing University of Traditional Chinese Medicine, Yancheng 224000, China – name: 5 Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China – name: 8 Zhejiang Provincial Key Laboratory for Diagnosis and Treatment of Aging and Physic-chemical Injury Diseases, 79 Qingchun Rd, Hangzhou 310003, China – name: 7 Department of Laboratory Medicine, The Central Blood Station of Yancheng City, Yancheng, 224000 Jiangsu, China – name: 2 Department of Laboratory Medicine, Yancheng Clinical Medical College of Nanjing Medical University, Yancheng 224001, China – name: 6 Department of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Shanghai 200065, China – name: 4 Medical School, Kunming University of Science and Technology, 727 Jing Ming South Road, Kunming 650031, China – name: 1 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Rd., Hangzhou 310003, China |
Author_xml | – sequence: 1 fullname: Jiang, Bin – sequence: 2 fullname: Yu, Jiong – sequence: 3 fullname: Cao, Hongcui – sequence: 4 fullname: Li, Lanjuan – sequence: 5 fullname: Yang, Jinfeng – sequence: 6 fullname: Shang, Anquan – sequence: 7 fullname: Wei, Daqiao – sequence: 8 fullname: Lv, Feifei – sequence: 9 fullname: Huang, Fen – sequence: 10 fullname: Lu, Xuan – sequence: 11 fullname: Guo, Yurong – sequence: 12 fullname: Wu, Jian – sequence: 13 fullname: Pan, Qiaoling |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33294465$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | Copyright © 2020 Jian Wu et al. COPYRIGHT 2020 John Wiley & Sons, Inc. Copyright © 2020 Jian Wu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 Copyright © 2020 Jian Wu et al. 2020 |
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Snippet | Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral... The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell... BACKGROUND AND AIMSThe involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral... |
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SubjectTerms | Antibodies Antibody Specificity - immunology Biomarkers CD3 antigen CD4 antigen Cell-mediated immunity Cytokines Cytokines - metabolism Disease Susceptibility Ethylenediaminetetraacetic acid Female Flow cytometry Health aspects Helper cells Hepatitis Hepatitis Antibodies - immunology Hepatitis E Hepatitis E - complications Hepatitis E - immunology Hepatitis E - metabolism Hepatitis E - virology Hepatitis E virus - immunology HIV Hospitals Human immunodeficiency virus Humans Immunoglobulin G Immunoglobulin M Immunology Infection Infections Interleukin 10 Interleukin 4 Liver Liver failure Liver Failure, Acute - diagnosis Liver Failure, Acute - etiology Lymphocytes Lymphocytes T Male Medical records Polymerase chain reaction Ribonucleic acid RNA RNA, Viral Severity of Illness Index Th1 Cells - immunology Th1 Cells - metabolism Th1 Cells - pathology Th2 Cells - immunology Th2 Cells - metabolism Th2 Cells - pathology Viral infections Viral Load Womens health γ-Interferon |
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Title | Th1/Th2 Cells and Associated Cytokines in Acute Hepatitis E and Related Acute Liver Failure |
URI | https://search.emarefa.net/detail/BIM-1187349 https://dx.doi.org/10.1155/2020/6027361 https://www.ncbi.nlm.nih.gov/pubmed/33294465 https://www.proquest.com/docview/2465228819 https://search.proquest.com/docview/2468662402 https://pubmed.ncbi.nlm.nih.gov/PMC7691005 https://doaj.org/article/75bc584732ce4ee3ad67103a69c2eba5 |
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