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Updated: Aug 16, 2025

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METTL3 Regulates the Inflammatory Response in CPB2 Toxin-Exposed IPEC-J2 Cells through the TLR2/NF-κB Signaling

Juanli Zhang1, Jiaojiao Yang1, Xiaoli Gao1

  • 1College of Animal Science and Technology, Gansu Agricultural University, Lanzhou 730070, China.

International Journal of Molecular Sciences
|December 23, 2022
PubMed

Insights

Methyltransferase-like 3 (METTL3) exacerbates intestinal inflammation caused by Clostridium perfringens beta2 toxin by activating the TLR2/NF-κB pathway. METTL3 may be a therapeutic target for C. perfringens-induced diarrhea.

Area of Science:

  • Molecular Biology
  • Immunology
  • Microbiology

Background:

  • Clostridium perfringens beta2 (CPB2) toxin causes intestinal diseases.
  • N6-methyladenosine (m6A) modification is crucial in disease.
  • Methyltransferase-like 3 (METTL3) influences immune responses to bacterial infections.

Purpose of the Study:

  • To investigate the role of METTL3 in CPB2-toxin-induced responses in porcine intestinal epithelial cells (IPEC-J2).

Main Methods:

  • Methylated RNA immunoprecipitation-quantitative polymerase chain reaction (MeRIP-qPCR)
  • Western blotting
  • Immunofluorescence assay

Main Results:

  • CPB2 toxin increased m6A and METTL3 levels in IPEC-J2 cells.
  • METTL3 overexpression enhanced inflammatory factor release, cytotoxicity, and disrupted tight junctions.
  • METTL3 knockdown reversed these effects.
  • METTL3 activated the TLR2/NF-κB signaling pathway by regulating TLR2 m6A levels.

Conclusions:

  • METTL3 promotes CPB2-induced inflammatory responses in IPEC-J2 cells via the TLR2/NF-κB pathway.
  • METTL3 may serve as a therapeutic target for C. perfringens-related diarrhea.
Keywords:
CPB2 toxinIPEC-J2METTL3TLR2/NF-κBinflammatory response

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