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microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment

INTRODUCTION: Human brucellosis is a zoonotic bacterial disease with up to 500,000 new cases each year. The major evasion mechanisms from the host immune system by Brucella are restraint of complement pathway and Toll‐like receptors signaling pathways, interference with efficient antigen presentatio...

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Autores principales: Kazemi, Sima, Mirzaei, Rasoul, Sholeh, Mohammad, Karampoor, Sajad, Keramat, Fariba, Saidijam, Massoud, Alikhani, Mohammad Yousef
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8589381/
https://www.ncbi.nlm.nih.gov/pubmed/34449979
http://dx.doi.org/10.1002/iid3.519
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author Kazemi, Sima
Mirzaei, Rasoul
Sholeh, Mohammad
Karampoor, Sajad
Keramat, Fariba
Saidijam, Massoud
Alikhani, Mohammad Yousef
author_facet Kazemi, Sima
Mirzaei, Rasoul
Sholeh, Mohammad
Karampoor, Sajad
Keramat, Fariba
Saidijam, Massoud
Alikhani, Mohammad Yousef
author_sort Kazemi, Sima
collection PubMed
description INTRODUCTION: Human brucellosis is a zoonotic bacterial disease with up to 500,000 new cases each year. The major evasion mechanisms from the host immune system by Brucella are restraint of complement pathway and Toll‐like receptors signaling pathways, interference with efficient antigen presentation to CD4‐positive T lymphocytes, selective subversion of autophagy pathways, inhibition of dendritic cell stimulation, inhibition of autophagolysosomal fusion, and macrophage apoptosis. Many molecular and cellular pathways contribute to brucellosis that microRNAs have a vital function in the immunopathogenesis of this disease. In this regard, these molecules apply for their roles by modulating various events like inflammatory reactions and immune defense. Recently, in the case of immunity to human brucellosis, it has been shown that microRNAs play an important role in immunity against these bacteria. METHODS AND RESULTS: In this study, we tried to review the immune defense and immunopathogenesis of Brucella infection and highlight the current knowledge of the microRNAs in infected cells by Brucella pathogens. The recent findings suggest that the regulation of microRNAs expression is impaired during brucellosis infection, which may contribute to disease progression or inhibition by modulating immune responses against this pathogen. CONCLUSIONS: The interplay between miRNAs and Brucella pathogens and the underlying process required comprehensive examination to unravel the novel therapeutic or diagnostic approaches.
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spelling pubmed-85893812021-11-19 microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment Kazemi, Sima Mirzaei, Rasoul Sholeh, Mohammad Karampoor, Sajad Keramat, Fariba Saidijam, Massoud Alikhani, Mohammad Yousef Immun Inflamm Dis Review Articles INTRODUCTION: Human brucellosis is a zoonotic bacterial disease with up to 500,000 new cases each year. The major evasion mechanisms from the host immune system by Brucella are restraint of complement pathway and Toll‐like receptors signaling pathways, interference with efficient antigen presentation to CD4‐positive T lymphocytes, selective subversion of autophagy pathways, inhibition of dendritic cell stimulation, inhibition of autophagolysosomal fusion, and macrophage apoptosis. Many molecular and cellular pathways contribute to brucellosis that microRNAs have a vital function in the immunopathogenesis of this disease. In this regard, these molecules apply for their roles by modulating various events like inflammatory reactions and immune defense. Recently, in the case of immunity to human brucellosis, it has been shown that microRNAs play an important role in immunity against these bacteria. METHODS AND RESULTS: In this study, we tried to review the immune defense and immunopathogenesis of Brucella infection and highlight the current knowledge of the microRNAs in infected cells by Brucella pathogens. The recent findings suggest that the regulation of microRNAs expression is impaired during brucellosis infection, which may contribute to disease progression or inhibition by modulating immune responses against this pathogen. CONCLUSIONS: The interplay between miRNAs and Brucella pathogens and the underlying process required comprehensive examination to unravel the novel therapeutic or diagnostic approaches. John Wiley and Sons Inc. 2021-08-27 /pmc/articles/PMC8589381/ /pubmed/34449979 http://dx.doi.org/10.1002/iid3.519 Text en © 2021 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Articles
Kazemi, Sima
Mirzaei, Rasoul
Sholeh, Mohammad
Karampoor, Sajad
Keramat, Fariba
Saidijam, Massoud
Alikhani, Mohammad Yousef
microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment
title microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment
title_full microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment
title_fullStr microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment
title_full_unstemmed microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment
title_short microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment
title_sort micrornas in human brucellosis: a promising therapeutic approach and biomarker for diagnosis and treatment
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8589381/
https://www.ncbi.nlm.nih.gov/pubmed/34449979
http://dx.doi.org/10.1002/iid3.519
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