Heat-not-burn tobacco products induce pro-inflammatory cytokines and oxidative stress, and alter gene expression in human dendritic cells

Clicks: 7
ID: 332473
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #157 of 160 articles by views in nicotine & tobacco research : official journal of the society for research on nicotine and tobacco

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 160 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Introduction Heat-not-burn (HNB) tobacco products generate aerosol by heating tobacco and are often perceived as less harmful than conventional cigarettes. However, their effects on human dendritic cells remain poorly understood. Methods Human monocyte-derived dendritic cells (moDCs) from three independent donors were exposed to HNB extract (HNBE) in immature or LPS-matured states. Surface phenotype, cytokine secretion, redox status, and transcriptomic responses were assessed. Selected RNA-seq findings were independently validated by RT-qPCR using moDCs from three additional independent donors. Results HNBE did not significantly alter DC-SIGN, HLA-DR, CD80, or CD86 expression. In LPS-matured moDCs, 30% HNBE increased IL-6 by approximately 1.3-fold and TNF-α by approximately 1.4-fold, whereas other measured cytokines remained unchanged. This preferential response may reflect the primed inflammatory state associated with LPS-induced maturation. HNBE also increased intracellular reactive oxygen species (ROS) and shifted cellular redox balance toward a more oxidized state. RNA sequencing identified 73 differentially expressed genes, including 28 upregulated and 45 downregulated genes, with enrichment of pathways related to immune signaling, antigen processing and presentation, and ribosomal processes. Key transcriptional changes, including those in THBS1, TIMP1, TREM1, and S100A9, were independently validated by RT-qPCR in an additional donor cohort. Conclusions HNBE selectively enhanced IL-6 and TNF-α secretion and disrupted redox homeostasis in LPS-matured human moDCs without substantially altering their surface-marker phenotype. These biological changes were accompanied by coordinated HNBE-associated transcriptional alterations, supporting further mechanistic and in vivo investigation of HNB-related immune effects. Implication This study provides human cell-based evidence that HNBE exposure can selectively enhance inflammatory responses and disrupt redox homeostasis in activated dendritic cells, accompanied by coordinated transcriptional alterations in immune-related pathways. These findings broaden current understanding of the immunological and redox effects of HNB products. Although further mechanistic and in vivo validation is required, the results highlight the importance of evaluating potential immune-related health effects when assessing the biological impact of HNB use.
Reference Key
openalex_W7222029080 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Yu-Chi Wang, Wen-Wei Lin, Wei-Lun Liu, Po‐Len Liu, Hsiao-Hsuan Wang, Sin‐Hua Moi, Hsiu-Lin Chen, I‐Ling Chen
Journal nicotine & tobacco research : official journal of the society for research on nicotine and tobacco
Year 2026
DOI
10.1093/ntr/ntag225
URL
https://doi.org/10.1093/ntr/ntag225
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.