ArticleFrontiers in immunology2021
L-Leucine Promotes STAT1 and ISGs Expression in TGEV-Infected IPEC-J2 Cells
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 15 citations in OpenAlex.
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- Quercetin Protects Against Transmissible Gastroenteritis Virus-Induced Intestinal Inflammation by Modulating Mitophagy-Driven Mitochondrial Dysfunction.International journal of biological sciences · 2025Article
- Advances research in porcine enteric coronavirus therapies and antiviral drugs.The veterinary quarterly · 2024Review
- Simultaneous Quantification of 66 Compounds in Two TibetanMolecules (Basel, Switzerland) · 2024Article
- Development and application of a quadruplexFrontiers in cellular and infection microbiology · 2024Article
- HSP90AB1 Is a Host Factor Required for Transmissible Gastroenteritis Virus Infection.International journal of molecular sciences · 2023Article
- Influenced tumor microenvironment and tumor immunity by amino acids.Frontiers in immunology · 2023Review
- Eugenol Attenuates Transmissible Gastroenteritis Virus-Induced Oxidative Stress and Apoptosis Via ROS-NRF2-ARE Signaling.Antioxidants (Basel, Switzerland) · 2022Article
- All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Apoptosis in IPEC-J2 Cells via Inhibiting ROS-Mediated PAntioxidants (Basel, Switzerland) · 2022Article
- Comparison of expression profiles between undifferentiated and differentiated porcine IPEC-J2 cells.Porcine health management · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
L-leucine (Leu), as one of the effective amino acids to activate the mTOR signaling pathway, can alleviate transmissible gastroenteritis virus (TGEV) infection. However, the underlying mechanism by which Leu alleviates the virus infection has not been fully characterized. In particular, how Leu impacts TGEV replication through mTOR signaling has yet to be elucidated. In the present study, we found that TGEV proliferated efficiently in intestinal porcine epithelial cells (IPEC-J2 cells) as evidenced by the increase in viral contents by flow cytometry, the inhibition of cell proliferation by CCK-8 assay as well as the reduction of PCNA level by western blot. Besides, western blot analysis showed that STAT1 expression was markedly reduced in TGEV-infected cells. The results of ELISA revealed the inhibition of ISGs (ISG56, MxA, and PKR) expressions by TGEV infection. TGEV-induced mTOR and its downstream p70 S6K and 4E-BP1, STAT1 and ISGs downregulation were blocked by an mTOR activator-MHY1485 but not by an mTOR inhibitor-RAPA. Concurrently, mTOR activation by MHY1485 reduced the contents of TGEV and vice versa. Furthermore, Leu reversed the inhibition of STAT1 and ISGs by activating mTOR and its downstream p70 S6K and 4E-BP1 in TEGV-infected cells. Our findings demonstrated that Leu promoted the expressions of STAT1 and ISGs
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