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Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile

Chronic hepatitis B (CHB) virus infection, causing immune dysfunction and chronic hepatitis, is one of the leading risk factors for hepatocellular cancer. We investigated how Arthrospira affected hepatitis B surface antigen (HBsAg) reduction in CHB patients under continued nucleos(t)ide analogues (N...

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Autores principales: Shiue, Sheng-Jie, Cheng, Chao-Ling, Shiue, Han-Shiang, Chen, Chun-Nan, Cheng, Sheng-Wei, Wu, Li-Wei, Jargalsaikhan, Ganbolor, Chan, Tze-Sian, Lin, Hsin-Yi, Wu, Ming-Shun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9325115/
https://www.ncbi.nlm.nih.gov/pubmed/35889747
http://dx.doi.org/10.3390/nu14142790
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author Shiue, Sheng-Jie
Cheng, Chao-Ling
Shiue, Han-Shiang
Chen, Chun-Nan
Cheng, Sheng-Wei
Wu, Li-Wei
Jargalsaikhan, Ganbolor
Chan, Tze-Sian
Lin, Hsin-Yi
Wu, Ming-Shun
author_facet Shiue, Sheng-Jie
Cheng, Chao-Ling
Shiue, Han-Shiang
Chen, Chun-Nan
Cheng, Sheng-Wei
Wu, Li-Wei
Jargalsaikhan, Ganbolor
Chan, Tze-Sian
Lin, Hsin-Yi
Wu, Ming-Shun
author_sort Shiue, Sheng-Jie
collection PubMed
description Chronic hepatitis B (CHB) virus infection, causing immune dysfunction and chronic hepatitis, is one of the leading risk factors for hepatocellular cancer. We investigated how Arthrospira affected hepatitis B surface antigen (HBsAg) reduction in CHB patients under continued nucleos(t)ide analogues (NA). Sixty CHB patients who had been receiving NA for at least one year with undetectable HBV DNA were randomized into three groups: control and oral Arthrospira at 3 or 6 g daily add-on therapy groups. Patients were followed up for 6 months. Oral Arthrospira-diet mice were established to investigate the possible immunological mechanism of Arthrospira against HBV. Within 6 months, mean quantitative HBsAg (qHBsAg) decreased in the oral Arthrospira add-on therapy group. Interestingly, interferon gamma (IFN-γ) increased but TNF-α, interleukin 6 (IL-6), hepatic fibrosis, and steatosis decreased in the add-on groups. In mice, Arthrospira enhanced both innate and adaptive immune system, especially natural killer (NK) cell cytotoxicity, B cell activation, and the interleukin 2 (IL-2), IFN-γ immune response. Arthrospira may modulate IL-2- and TNF-α/IFN-γ-mediated B and T cell activation to reduce HBsAg. Also, Arthrospira has the potential to restore immune tolerance and enhance HBsAg seroclearance in CHB patients through promoting T, B, and NK cell activation.
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spelling pubmed-93251152022-07-27 Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile Shiue, Sheng-Jie Cheng, Chao-Ling Shiue, Han-Shiang Chen, Chun-Nan Cheng, Sheng-Wei Wu, Li-Wei Jargalsaikhan, Ganbolor Chan, Tze-Sian Lin, Hsin-Yi Wu, Ming-Shun Nutrients Article Chronic hepatitis B (CHB) virus infection, causing immune dysfunction and chronic hepatitis, is one of the leading risk factors for hepatocellular cancer. We investigated how Arthrospira affected hepatitis B surface antigen (HBsAg) reduction in CHB patients under continued nucleos(t)ide analogues (NA). Sixty CHB patients who had been receiving NA for at least one year with undetectable HBV DNA were randomized into three groups: control and oral Arthrospira at 3 or 6 g daily add-on therapy groups. Patients were followed up for 6 months. Oral Arthrospira-diet mice were established to investigate the possible immunological mechanism of Arthrospira against HBV. Within 6 months, mean quantitative HBsAg (qHBsAg) decreased in the oral Arthrospira add-on therapy group. Interestingly, interferon gamma (IFN-γ) increased but TNF-α, interleukin 6 (IL-6), hepatic fibrosis, and steatosis decreased in the add-on groups. In mice, Arthrospira enhanced both innate and adaptive immune system, especially natural killer (NK) cell cytotoxicity, B cell activation, and the interleukin 2 (IL-2), IFN-γ immune response. Arthrospira may modulate IL-2- and TNF-α/IFN-γ-mediated B and T cell activation to reduce HBsAg. Also, Arthrospira has the potential to restore immune tolerance and enhance HBsAg seroclearance in CHB patients through promoting T, B, and NK cell activation. MDPI 2022-07-06 /pmc/articles/PMC9325115/ /pubmed/35889747 http://dx.doi.org/10.3390/nu14142790 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Shiue, Sheng-Jie
Cheng, Chao-Ling
Shiue, Han-Shiang
Chen, Chun-Nan
Cheng, Sheng-Wei
Wu, Li-Wei
Jargalsaikhan, Ganbolor
Chan, Tze-Sian
Lin, Hsin-Yi
Wu, Ming-Shun
Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile
title Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile
title_full Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile
title_fullStr Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile
title_full_unstemmed Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile
title_short Arthrospira Enhances Seroclearance in Patients with Chronic Hepatitis B Receiving Nucleos(t)ide Analogue through Modulation of TNF-α/IFN-γ Profile
title_sort arthrospira enhances seroclearance in patients with chronic hepatitis b receiving nucleos(t)ide analogue through modulation of tnf-α/ifn-γ profile
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9325115/
https://www.ncbi.nlm.nih.gov/pubmed/35889747
http://dx.doi.org/10.3390/nu14142790
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