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Role of NLRP3 Inflammasome in Inflammatory and Immunological Diseases

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Dear Colleagues,

The NLRP3 inflammasome is a multimeric protein complex machinery consisting of three subunits: the sensor-NLRP3, an adaptor-ASC subunit, and the effector-caspase-1. Caspase-1 converts the pro-inflammatory cytokine pro-IL1B to the active form IL1B. Recent studies have elucidated the role of the inflammasome in various inflammatory and immunological diseases. A common theme among these diseases is the correlation between increased levels of NLRP3 and/or its product IL1B and the worsening of the disease.

Based on these observations, many studies have suggested targeting the NLRP3 inflammasome as a strategy for designing new therapeutic drug molecules. However, there remain several unanswered questions that need to be addressed, such as whether the NLRP3 inflammasome is a common target for the inflammatory state of the disease and whether we are close to finding a treatment by reducing the inflammation.

In this review, we aim to comprehensively cover all known relevant information about the NLRP3 inflammasome. This includes its structure, the different pathways involved (canonical and non-canonical), its roles in various inflammatory or immunological diseases, and how targeting the NLRP3 inflammasome can serve as a key strategy to uncover hidden secrets and pave the way for potential therapeutic interventions.

In this Special Issue, original research articles and reviews are welcome.

I look forward to receiving your contributions.

Dr. Sunny Malhotra
Guest Editor

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Keywords

NLRP3 inflammasome
immunological diseases
therapeutic target
inflammation
immune-response

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13 pages, 2659 KiB

Open AccessArticle

Chronic HIV Infection Increases Monocyte NLRP3 Inflammasome-Dependent IL-1α and IL-1β Release

by Hedda Hoel, Tuva Børresdatter Dahl, Kuan Yang, Linda Gail Skeie, Annika Elisabet Michelsen, Thor Ueland, Jan Kristian Damås, Anne Ma Dyrhol-Riise, Børre Fevang, Arne Yndestad, Pål Aukrust, Marius Trøseid and Øystein Sandanger

Int. J. Mol. Sci. 2024, 25(13), 7141; https://doi.org/10.3390/ijms25137141 - 28 Jun 2024

Viewed by 498

Abstract

Antiretroviral treatment (ART) has converted HIV from a lethal disease to a chronic condition, yet co-morbidities persist. Incomplete immune recovery and chronic immune activation, especially in the gut mucosa, contribute to these complications. Inflammasomes, multi-protein complexes activated by innate immune receptors, appear to play a role in these inflammatory responses. In particular, preliminary data indicate the involvement of IFI16 and NLRP3 inflammasomes in chronic HIV infection. This study explores inflammasome function in monocytes from people with HIV (PWH); 22 ART-treated with suppressed viremia and 17 untreated PWH were compared to 33 HIV-negative donors. Monocytes were primed with LPS and inflammasomes activated with ATP in vitro. IFI16 and NLRP3 mRNA expression were examined in a subset of donors. IFI16 and NLRP3 expression in unstimulated monocytes correlated negatively with CD4 T cell counts in untreated PWH. For IFI16, there was also a positive correlation with viral load. Monocytes from untreated PWH exhibit increased release of IL-1α, IL-1β, and TNF compared to treated PWH and HIV-negative donors. However, circulating monocytes in PWH are not pre-primed for inflammasome activation in vivo. The findings suggest a link between IFI16, NLRP3, and HIV progression, emphasizing their potential role in comorbidities such as cardiovascular disease. The study provides insights into inflammasome regulation in HIV pathogenesis and its implications for therapeutic interventions. Full article

(This article belongs to the Special Issue Role of NLRP3 Inflammasome in Inflammatory and Immunological Diseases)

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Role of NLRP3 Inflammasome in Inflammatory and Immunological Diseases

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