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Review
. 2023 Apr 18:14:1178434.
doi: 10.3389/fimmu.2023.1178434. eCollection 2023.

NLRP3 inflammasome as a sensor of micro- and nanoplastics immunotoxicity

Andi Alijagic  1   2   3 , Alexander Hedbrant  1   2 , Alexander Persson  1   2 , Maria Larsson  3 , Magnus Engwall  3 , Eva Särndahl  1   2
Affiliations
Review

NLRP3 inflammasome as a sensor of micro- and nanoplastics immunotoxicity

Andi Alijagic et al. Front Immunol. .

Abstract

Micro- and nanoplastics (MNPs) are emerging pollutants with scarcely investigated effects on human innate immunity. If they follow a similar course of action as other, more thoroughly investigated particulates, MNPs may penetrate epithelial barriers, potentially triggering a cascade of signaling events leading to cell damage and inflammation. Inflammasomes are intracellular multiprotein complexes and stimulus-induced sensors critical for mounting inflammatory responses upon recognition of pathogen- or damage-associated molecular patterns. Among these, the NLRP3 inflammasome is the most studied in terms of activation via particulates. However, studies delineating the ability of MNPs to affect NLRP3 inflammasome activation are still rare. In this review, we address the issue of MNPs source and fate, highlight the main concepts of inflammasome activation via particulates, and explore recent advances in using inflammasome activation for assessment of MNP immunotoxicity. We also discuss the impact of co-exposure and MNP complex chemistry in potential inflammasome activation. Development of robust biological sensors is crucial in order to maximize global efforts to effectively address and mitigate risks that MNPs pose for human health.

Keywords: human health; inflammation; innate immunity; plastics; pollution.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Interplay between micro- and nanoplastics (MNPs) and NLRP3 inflammasome canonical activation pathway. Left panel – major sources and properties of MNPs. MNPs may be unintentionally released or deliberately added to different products. MNPs significantly vary in terms of physicochemical properties, including size, shape, and chemical composition. Importantly, MNPs may act as a vector of various environmental contaminants, such as persistent organic pollutants (POPs), heavy metals, or pathogenic bacteria. PAHs – polycyclic aromatic hydrocarbons; PFAS – Per- and polyfluoroalkyl substances. Middle panel – the main MNP exposure routes in humans include inhalation and ingestion leading to MNP interaction with alveolar and intestinal epithelia. Right panel – Putative mechanisms of MNP-mediated activation of NLRP3 inflammasome in the immunocompetent cells, including Toll-like receptor (TLR)-priming via NF-κB resulting in production of NLRP3 inflammasome components, and NLRP3 inflammasome activation leading to the recruitment of the caspase-1 that cleaves its effector substrates, pro-Interleukin-1β (pro-IL-1β), pro-IL-18, and gasdermin-D (GSDMD). The main outcomes of the NLRP3 inflammasome activation include maturation and release of IL-1β and IL-18, and pro-inflammatory cell death (pyroptosis). Figure was created by AA using BioRender.com.
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This work was supported by the Swedish Knowledge Foundation (Grants No. 20160019; 20190107; 20200017; 20220122; 20160044).

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