# Type I Interferon-Enhancing Effect of Cardamom Seed Extract via Intracellular Nucleic Acid Sensor Regulation

**Authors:** Abdullah Al Sufian Shuvo, Masahiro Kassai, Takeshi Kawahara

PMC · DOI: 10.3390/foods14152744 · Foods · 2025-08-06

## TL;DR

Cardamom seed extract boosts type I interferon production, which may help prevent viral infections by regulating nucleic acid sensors in cells.

## Contribution

This study reveals that cardamom seed extract enhances type I IFN responses via nucleic acid sensors, with distinct mechanisms involving STING and TCDD-inducible poly-ADP-ribose polymerase.

## Key findings

- CSWE and 1,8-cineole induce type I IFNs and IFN-stimulated genes in A549 cells transfected with nucleic acids.
- CSWE's effect is STING-dependent, while 1,8-cineole's effect is STING-independent and involves down-regulation of TCDD-inducible poly-ADP-ribose polymerase.
- CSWE may act as an antiviral agent by enhancing homeostatic type I IFN production.

## Abstract

The induction of type I interferon (IFN) via intracellular nucleic acid sensors may be useful in preventing viral infections. However, little is known about the effect of natural plant materials on sensor responses. We previously found that cardamom (Elettaria cardamomum (L.) Maton) seed extract (CSWE) enhanced type I IFN expression and prevented influenza virus infection. In this study, we investigated the effect of CSWE on type I IFN responses using intracellular nucleic acid sensor molecules. Human lung epithelial A549 cells were treated with CSWE and transfected with poly(dA:dT) or poly(I:C) using lipofection. CSWE and 1,8-cineole, the major CSWE components, dose-dependently induced type I IFNs and IFN-stimulated genes in both poly(dA:dT)- and poly(I:C)-transfected A549 cells. The type I IFN-enhancing effect of CSWE was dependent on the stimulator of interferon genes (STING), whereas the effect of 1,8-cineole was independent of STING and mediated by the down-regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose polymerase expression. Our study suggests that CSWE has the potential to act as a beneficial antiviral agent by enhancing homeostatic type I IFN production.

## Linked entities

- **Genes:** STING1 (stimulator of interferon response cGAMP interactor 1) [NCBI Gene 340061]
- **Chemicals:** 1,8-cineole (PubChem CID 2758)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** IFNA1 (interferon alpha 1) [NCBI Gene 3439] {aka IFL, IFN, IFN-ALPHA, IFN-alphaD, IFNA13, IFNA@}, PARP1 (poly(ADP-ribose) polymerase 1) [NCBI Gene 142] {aka ADPRT, ADPRT 1, ADPRT1, ARTD1, PARP, PARP-1}, STING1 (stimulator of interferon response cGAMP interactor 1) [NCBI Gene 340061] {aka ERIS, MITA, MPYS, NET23, SAVI, STING}
- **Diseases:** influenza virus infection (MESH:D007251), viral infections (MESH:D014777)
- **Chemicals:** 2,3,7,8-tetrachlorodibenzo-p-dioxin (MESH:D000072317), 1,8-cineole (MESH:D000077591), poly(dA:dT) (MESH:D011067), CSWE (-), poly(I:C) (MESH:D011070)
- **Species:** Homo sapiens (human, species) [taxon 9606], Elettaria cardamomum (cardamom, species) [taxon 105181]
- **Cell lines:** A549 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0023)

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12346419/full.md

## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12346419/full.md

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Source: https://tomesphere.com/paper/PMC12346419