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NLRP3 炎性小体在麻风病中的表达表明麻风分枝杆菌的免疫逃避。

Expression of NLRP3 inflammasome in leprosy indicates immune evasion of Mycobacterium leprae.

机构信息

Universidade Federal de Minas Gerais, Faculdade de Medicina, Departamento de Anatomia Patológica e Medicina Legal, Belo Horizonte, MG, Brasil.

Universidade Federal de Minas Gerais, Faculdade de Medicina, Departamento de Clínica Médica, Belo Horizonte, MG, Brasil.

出版信息

Mem Inst Oswaldo Cruz. 2020 Feb 27;115:e190324. doi: 10.1590/0074-02760190324. eCollection 2020.

DOI:10.1590/0074-02760190324
PMID:32130367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7046136/
Abstract

BACKGROUND

Leprosy is an infectious-contagious disease caused by Mycobacterium leprae that remain endemic in 105 countries. This neglected disease has a wide range of clinical and histopathological manifestations that are related to the host inflammatory and immune responses. More recently, the inflammasome has assumed a relevant role in the inflammatory response against microbiological agents. However, the involvement of inflammasome in leprosy remains poorly understood.

OBJECTIVES

The aim is to associate biomarkers of inflammasome with the different immunopathological forms of leprosy.

METHODS

We performed an observational, cross-sectional, and comparative study of the immunophenotypic expression of inflammasome-associated proteins in immunopathological forms of leprosy of 99 skin lesion samples by immunohistochemistry. The intensity and percentage of NLRP3, Caspase-1, Caspases-4/5, interleukin-1β and interleukin-18 immunoreactivities in the inflammatory infiltrate of skin biopsies were evaluated.

FINDINGS

Strong expression of NLRP3 and inflammatory Caspases-4/5 were observed in lepromatous leprosy (lepromatous pole). In addition, were observed low expression of caspase-1, interleukin-1β, and interleukin-18 in tuberculoid and lepromatous leprosy. The interpolar or borderline form showed immunophenotype predominantly similar to the lepromatous pole.

MAIN CONCLUSIONS

Our results demonstrate that the NLRP3 inflammasome is inactive in leprosy, suggesting immune evasion of M. leprae.

摘要

背景

麻风病是一种由麻风分枝杆菌引起的传染性疾病,在 105 个国家仍呈地方性流行。这种被忽视的疾病具有广泛的临床和组织病理学表现,与宿主的炎症和免疫反应有关。最近,炎症小体在针对微生物病原体的炎症反应中发挥了重要作用。然而,炎症小体在麻风病中的作用仍知之甚少。

目的

旨在将炎症小体的生物标志物与麻风病的不同免疫病理学形式联系起来。

方法

我们通过免疫组织化学方法对 99 例皮肤病变样本中麻风病免疫病理学形式的炎症小体相关蛋白的免疫表型表达进行了观察性、横断面和比较研究。评估了 NLRP3、Caspase-1、Caspases-4/5、白细胞介素-1β和白细胞介素-18 免疫反应性在皮肤活检炎症浸润中的强度和百分比。

结果

在瘤型麻风(瘤型极点)中观察到 NLRP3 和炎症 Caspases-4/5 的强表达。此外,在结核样型和瘤型麻风中观察到 Caspase-1、白细胞介素-1β和白细胞介素-18 的低表达。交界型或边界型表现出的免疫表型主要类似于瘤型极点。

主要结论

我们的结果表明,NLRP3 炎症小体在麻风病中不活跃,提示麻风分枝杆菌的免疫逃避。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f29/7046136/ae5ba7a0819c/1678-8060-mioc-115-e190324-gf2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f29/7046136/3bfe11d59951/1678-8060-mioc-115-e190324-gf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f29/7046136/ae5ba7a0819c/1678-8060-mioc-115-e190324-gf2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f29/7046136/3bfe11d59951/1678-8060-mioc-115-e190324-gf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f29/7046136/ae5ba7a0819c/1678-8060-mioc-115-e190324-gf2.jpg

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