HIV-1 induces the first signal to activate the NLRP3 inflammasome in monocyte-derived macrophages
Background/Aims: Inflammasomes are multimolecular complexes that regulate caspase-1. They act as sensors for endogenous and exogenous signals, and mediate the processing of pro-IL-1ß into its secreted, biologically active form. The NLRP3 inflammasome and IL-1ß are particularly interesting because th...
- Autores:
-
Hernández López, Juan Carlos
Latz E.
Urcuqui-Inchima S.
- Tipo de recurso:
- Article of journal
- Fecha de publicación:
- 2013
- Institución:
- Universidad Cooperativa de Colombia
- Repositorio:
- Repositorio UCC
- Idioma:
- OAI Identifier:
- oai:repository.ucc.edu.co:20.500.12494/41805
- Palabra clave:
- cryopyrin
immunoglobulin enhancer binding protein
inflammasome
interleukin 1beta
immunoglobulin enhancer binding protein
interleukin 1beta
article
controlled study
cytokine release
enzyme linked immunosorbent assay
human
human cell
Human immunodeficiency virus 1 infection
macrophage
priority journal
protein induction
signal transduction
virus envelope
Article
envelope gene
Human immunodeficiency virus 1
Human immunodeficiency virus 1 infection
macrophage
monocyte
nonhuman
Carrier Proteins
Cells
Cultured
Enzyme-Linked Immunosorbent Assay
HIV-1
Humans
Inflammasomes
Interleukin-1beta
Macrophages
Human immunodeficiency virus 1
- Rights
- closedAccess
- License
- http://purl.org/coar/access_right/c_14cb
Summary: | Background/Aims: Inflammasomes are multimolecular complexes that regulate caspase-1. They act as sensors for endogenous and exogenous signals, and mediate the processing of pro-IL-1ß into its secreted, biologically active form. The NLRP3 inflammasome and IL-1ß are particularly interesting because they are required for efficient control of viral infections. Indeed, HIV-1 induces expression of NLRP3 and IL-1ß in healthy controls, but not in HIV-1-infected patients. Here we evaluate whether HIV-1 can induce activation of the NLRP3 inflammasome. Methods: Human primary monocyte-derived macrophages were infected with HIV-1 in the absence or presence of classical NLRP3 inflammasome activators, and IL-1ß release was assessed by ELISA. Results: HIV-1 initiates the priming signal for NLRP3 inflammasome activation through the NF-?B-associated pathway in human primary monocyte-derived macrophages. Furthermore, priming of NLRP3 activation in response to HIV-1 was independent of the viral envelope, since similar results were observed with HIV-1 and pseudotyped HIV-1 lacking the env gene. Conclusion: Our findings suggest that HIV-1 infection promotes IL-1ß secretion by inducing the first signal for NLRP3 inflammasome activation, a phenomenon that may contribute to AIDS progression. Copyright © 2013 S. Karger AG, Basel. |
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