What question did this study set out to answer?

This research aims to understand the cellular responses to welding particles and their toxicity mechanisms in lung cells.

May 6, 2026

91 Transcriptomic profiling reveals immunomodulatory effects of welding particles in lung epithelial and macrophage-like cells

Key Points

This research aims to understand the cellular responses to welding particles and their toxicity mechanisms in lung cells.
Investigated welding particles from mild steel and stainless steel in human bronchial epithelial and macrophage-like cells.
Confirmed cellular uptake using transmission electron microscopy and quantified metal content via ICP-MS.
Conducted bulk RNA sequencing to assess differentially expressed genes across the cell types and particle types.
Performed validation experiments to measure cytokine secretion and DNA damage.
Utilized single-cell RNA sequencing to evaluate cell-cell interactions and inflammatory responses.
Demonstrated dose- and time-dependent reductions in metabolic activity, particularly with stainless steel.
Revealed more differentially expressed genes in macrophage-like THP-1 cells compared to lung epithelial BEAS-2B cells.
Showed strong enrichment of immune response pathways activated in THP-1 cells and moderate effects in BEAS-2B cells.
Confirmed increased cytokine secretion and DNA damage in THP-1 cells exposed to welding particles, with stronger effects from stainless steel.
Indicated that co-culture with macrophage-like cells promotes a pro-inflammatory phenotype in BEAS-2B cells, highlighting significant cell-cell interactions.

Abstract

Abstract Welding fumes contain respirable particles rich in metals (eg iron, manganese, chromium, nickel) and are classified as Group 1 carcinogens by IARC. Despite epidemiological evidence linking welding fume exposure to increased lung cancer risk, underlying molecular mechanisms remain poorly understood. This study investigates acute toxicity and transcriptomic responses to welding particles from mild steel (MS) and stainless steel (SS) generated via gas-metal arc welding in human bronchial epithelial cells (BEAS-2B) and macrophage-like cells (THP-1). Cellular uptake was confirmed by TEM and quantified by ICP-MS, revealing similar metal content for the two cell types. Dose- and time-dependent reductions in metabolic activity were identified, particularly for SS. Bulk RNAseq revealed more differentially expressed genes (DEGs) in THP-1 compared to BEAS-2B cells and more DEGs for SS compared to MS. Pathways related to immune response were strongly enriched and activated in THP-1 cells for both particles and moderately activated or inhibited in BEAS-2B cells. Validation experiments confirmed increased cytokine secretion and DNA damage in THP-1 cells with stronger effects for SS. Both particles reduced cytokine secretion in BEAS-2B cells indicating an immunomodulatory response. To understand the role of cell-cell interactions in mediating the response we performed single-cell RNAseq after exposure to BEAS-2B and THP-1 in co-culture. BEAS-2B cells acquired a pro-inflammatory phenotype (eg increased CXCL8 in response to SS) when co-cultured with THP-1 cells compared to monoculture. Overall, our data highlights distinct cellular responses to welding particles and underscores the importance of particle composition, cell type and cell-cell interactions in mediating toxicity.

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