# Activation of the NALP3-CASP1-IL-1 β Inflammatory Pathway by Pesticide Exposure in Human Umbilical Vein Endothelial Cells

**Authors:** Antonella Mazzone, Ylenia Della Rocca, Federica Flamminii, Simone Guarnieri, Dainelys Guadarrama Bello, Antonio Nanci, Oriana Trubiani, Francesca Diomede, Jacopo Pizzicannella

PMC · DOI: 10.3390/ijms26104947 · International Journal of Molecular Sciences · 2025-05-21

## TL;DR

This study shows that pesticides can activate an inflammatory pathway in blood vessel cells, leading to potential vascular damage and prolonged inflammation.

## Contribution

The study demonstrates pesticide-induced activation of the NALP3-CASP1-IL-1β pathway in endothelial cells, linking it to necroptosis and inflammation.

## Key findings

- Pesticide exposure activates the NALP3-CASP1-IL-1β inflammatory pathway in HUVECs.
- Pesticides induce ROS generation and morphological changes in endothelial cells.
- Exposure may lead to necroptosis and prolonged inflammation in vascular cells.

## Abstract

Barrier function regulation, angiogenic potential, and immune response modulation are only a few of the many roles of the vascular system that nowadays represent one of the main targets for environmental pollutants, in particular, pesticides. We have used human umbilical vein endothelial cells (HUVECs) as an in vitro model to investigate the effects of pesticides on the activation of the NALP3-CASP1-IL-1β inflammatory pathway using real time PCR (RT-PCR) and immunofluorescence investigations, reactive oxygen species (ROS) generation, and morphological alterations with scanning electron microscopy (SEM) analysis. Our findings offer a comprehensive evaluation of the cellular and molecular damage induced by pesticide exposure and show strong inflammasome activation. They indicate that these chemicals may initiate necroptosis and drive prolonged inflammation in endothelial cells. This study provides crucial insights into how pesticides contribute to endothelial dysfunction, highlighting the need for further investigation into their inflammatory and immune-modulatory effects on vascular health.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], CASP1 (caspase 1) [NCBI Gene 834], IL1B (interleukin 1 beta) [NCBI Gene 3553]
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, CASP1 (caspase 1) [NCBI Gene 834] {aka ICE, IL1BC, P45}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}
- **Diseases:** endothelial dysfunction (MESH:D014652), Inflammatory (MESH:D007249)
- **Chemicals:** ROS (MESH:D017382)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

17 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12111847/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12111847/full.md

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Source: https://tomesphere.com/paper/PMC12111847