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Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis

Mycobacterium leprae causes leprosy, a dermatoneurological disease which affects the skin and peripheral nerves. One of several cellular structures affected during M. leprae infection is the endoplasmic reticulum (ER). Infection by microorganisms can result in ER stress and lead to the accumulation...

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Autores principales: Hirai, Kelly Emi, de Sousa, Jorge Rodrigues, Silva, Luciana Mota, Junior, Leônidas Braga Dias, Furlaneto, Ismari Perini, Carneiro, Francisca Regina Oliveira, de Souza Aarão, Tinara Leila, Sotto, Mirian Nacagami, Quaresma, Juarez Antonio Simões
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6311872/
https://www.ncbi.nlm.nih.gov/pubmed/30647798
http://dx.doi.org/10.1155/2018/7067961
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author Hirai, Kelly Emi
de Sousa, Jorge Rodrigues
Silva, Luciana Mota
Junior, Leônidas Braga Dias
Furlaneto, Ismari Perini
Carneiro, Francisca Regina Oliveira
de Souza Aarão, Tinara Leila
Sotto, Mirian Nacagami
Quaresma, Juarez Antonio Simões
author_facet Hirai, Kelly Emi
de Sousa, Jorge Rodrigues
Silva, Luciana Mota
Junior, Leônidas Braga Dias
Furlaneto, Ismari Perini
Carneiro, Francisca Regina Oliveira
de Souza Aarão, Tinara Leila
Sotto, Mirian Nacagami
Quaresma, Juarez Antonio Simões
author_sort Hirai, Kelly Emi
collection PubMed
description Mycobacterium leprae causes leprosy, a dermatoneurological disease which affects the skin and peripheral nerves. One of several cellular structures affected during M. leprae infection is the endoplasmic reticulum (ER). Infection by microorganisms can result in ER stress and lead to the accumulation of unfolded or poorly folded proteins. To restore homeostasis in the cell, the cell induces a series of signaling cascades known as the unfolded protein response called UPR (unfolded protein response). The present work is aimed at investigating the in situ expression of these markers in cutaneous lesions of clinical forms of leprosy and establish possible correlation expression patterns and types of lesion. A total of 43 samples from leprosy patients were analyzed by immunohistochemistry with monoclonal antibodies against GRP78/BiP, PERK, IRE1α, and ATF6. A statistically significant difference between the indeterminate, tuberculoid, and lepromatous clinical forms was detected, with high expression of GRP78/BiP, PERK, IRE1α, and ATF6 in tuberculoid forms (TT) when compared to lepromatous leprosy (LL) and indeterminate (I) leprosy. These results represent the first evidence of ER stress in samples of skin lesions from leprosy patients. We believe that they will provide better understanding of the complex pathogenesis of the disease and facilitate further characterization of the cascade of molecular events elicited during infection.
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spelling pubmed-63118722019-01-15 Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis Hirai, Kelly Emi de Sousa, Jorge Rodrigues Silva, Luciana Mota Junior, Leônidas Braga Dias Furlaneto, Ismari Perini Carneiro, Francisca Regina Oliveira de Souza Aarão, Tinara Leila Sotto, Mirian Nacagami Quaresma, Juarez Antonio Simões Dis Markers Research Article Mycobacterium leprae causes leprosy, a dermatoneurological disease which affects the skin and peripheral nerves. One of several cellular structures affected during M. leprae infection is the endoplasmic reticulum (ER). Infection by microorganisms can result in ER stress and lead to the accumulation of unfolded or poorly folded proteins. To restore homeostasis in the cell, the cell induces a series of signaling cascades known as the unfolded protein response called UPR (unfolded protein response). The present work is aimed at investigating the in situ expression of these markers in cutaneous lesions of clinical forms of leprosy and establish possible correlation expression patterns and types of lesion. A total of 43 samples from leprosy patients were analyzed by immunohistochemistry with monoclonal antibodies against GRP78/BiP, PERK, IRE1α, and ATF6. A statistically significant difference between the indeterminate, tuberculoid, and lepromatous clinical forms was detected, with high expression of GRP78/BiP, PERK, IRE1α, and ATF6 in tuberculoid forms (TT) when compared to lepromatous leprosy (LL) and indeterminate (I) leprosy. These results represent the first evidence of ER stress in samples of skin lesions from leprosy patients. We believe that they will provide better understanding of the complex pathogenesis of the disease and facilitate further characterization of the cascade of molecular events elicited during infection. Hindawi 2018-12-16 /pmc/articles/PMC6311872/ /pubmed/30647798 http://dx.doi.org/10.1155/2018/7067961 Text en Copyright © 2018 Kelly Emi Hirai et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Hirai, Kelly Emi
de Sousa, Jorge Rodrigues
Silva, Luciana Mota
Junior, Leônidas Braga Dias
Furlaneto, Ismari Perini
Carneiro, Francisca Regina Oliveira
de Souza Aarão, Tinara Leila
Sotto, Mirian Nacagami
Quaresma, Juarez Antonio Simões
Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
title Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
title_full Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
title_fullStr Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
title_full_unstemmed Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
title_short Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
title_sort endoplasmic reticulum stress markers and their possible implications in leprosy's pathogenesis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6311872/
https://www.ncbi.nlm.nih.gov/pubmed/30647798
http://dx.doi.org/10.1155/2018/7067961
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