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Updated: Dec 27, 2025
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Expression of NLRP3 inflammasome in leprosy indicates immune evasion of Mycobacterium leprae
Ana Luisa Gomes Mendes1, Heloísa Di Matteo Joaquim1, Mara Inês Stefanini Zamae1
1Universidade Federal de Minas Gerais, Faculdade de Medicina, Departamento de Anatomia Patológica e Medicina Legal, Belo Horizonte, MG, Brasil.
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.
