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Peer-reviewedCC BY 4.0Frontiers in Pharmacology

Pretreatment with Commelina communis L. improves survival following influenza a virus infection and enhances innate interferon signaling

  1. 1Korean Medicine Application Center, Korea Institute of Oriental Medicine
  2. 2Cell and Matrix Research Institute, School of Medicine, Kyungpook National University
  3. 3College of Medicine, Chungnam National University

Abstract

The objectives of this study were to evaluate the pre-exposure protective effects of Commelina communis L. (CCL) against influenza A virus (IAV) infection and to investigate its associated immunomodulatory mechanisms. Using RAW 264.7 cells and BALB/c mouse models, we demonstrated that CCL pretreatment reduced viral replication markers and suppressed viral protein expression in vitro . In vivo , prophylactic administration of CCL improved survival from 0% to 40% and attenuated body-weight loss following IAV challenge. Mechanistically, CCL enhanced the secretion of type I interferon IFN-β through activation of TANK-binding kinase 1 (TBK1) and interferon regulatory factors 3 and 7 (IRF3/7). Activation of this signaling pathway was associated with STAT1/2 phosphorylation and increased expression of antiviral interferon-stimulated genes, including Isg20 and Isg56 . Phytochemical profiling using ultra-high-performance liquid chromatography coupled with quadrupole-Orbitrap high-resolution mass spectrometry (UHPLC-UV-HRMS) identified four phytochemicals in CCL, among which rutin showed the greatest activity among the tested compounds in the in vitro screening assay. Collectively, these findings suggest that CCL and rutin may enhance host antiviral defense by modulating innate interferon signaling when administered before IAV exposure period.

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BibTeX
@article{kwon2026pretreatment,
  title = {{Pretreatment with Commelina communis L. improves survival following influenza a virus infection and enhances innate interferon signaling}},
  author = {Eun-Bin Kwon and Hye Jin Yang and Buyun Kim and Wei Li and Young Eun Kim and Young Soo Kim and Jang-gi Choi},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = nov,
  doi = {10.3389/fphar.2026.1924427},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1924427/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Pretreatment with Commelina communis L. improves survival following influenza a virus infection and enhances innate interferon signaling
AU  - Eun-Bin Kwon
AU  - Hye Jin Yang
AU  - Buyun Kim
AU  - Wei Li
AU  - Young Eun Kim
AU  - Young Soo Kim
AU  - Jang-gi Choi
PY  - 2026
DA  - 2026/11/03
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.1924427
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.1924427/full
AB  - The objectives of this study were to evaluate the pre-exposure protective effects of Commelina communis L. (CCL) against influenza A virus (IAV) infection and to investigate its associated immunomodulatory mechanisms. Using RAW 264.7 cells and BALB/c mouse models, we demonstrated that CCL pretreatment reduced viral replication markers and suppressed viral protein expression in vitro . In vivo , prophylactic administration of CCL improved survival from 0% to 40% and attenuated body-weight loss following IAV challenge. Mechanistically, CCL enhanced the secretion of type I interferon IFN-β through activation of TANK-binding kinase 1 (TBK1) and interferon regulatory factors 3 and 7 (IRF3/7). Activation of this signaling pathway was associated with STAT1/2 phosphorylation and increased expression of antiviral interferon-stimulated genes, including Isg20 and Isg56 . Phytochemical profiling using ultra-high-performance liquid chromatography coupled with quadrupole-Orbitrap high-resolution mass spectrometry (UHPLC-UV-HRMS) identified four phytochemicals in CCL, among which rutin showed the greatest activity among the tested compounds in the in vitro screening assay. Collectively, these findings suggest that CCL and rutin may enhance host antiviral defense by modulating innate interferon signaling when administered before IAV exposure period.
SN  - 1663-9812
ER  -