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Thioredoxin-interacting protein-derived peptide (TN13) inhibits LPS-induced inflammation by inhibiting p38 MAPK

Dong Oh Kim1, Jae-Eun Byun2, Hyun-A Seong3

  • 1Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Yuseong-gu, Daejeon, 34141, Republic of Korea.

Biochemical and Biophysical Research Communications
|November 19, 2018
PubMed

Insights

Thioredoxin-interacting protein-derived peptide (TN13), conjugated to HIV trans-activator protein (TAT-TN13), effectively reduces macrophage inflammation by inhibiting the p38 MAPK pathway. This peptide shows potential as a novel therapeutic for inflammation-related diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Inflammation is a critical innate immune response mediated by macrophages.
  • The p38 mitogen-activated protein kinase (MAPK) pathway plays a central role in regulating macrophage inflammatory responses.
  • Identifying novel therapeutic targets for inflammation-related diseases is crucial.

Purpose of the Study:

  • To investigate the anti-inflammatory effects of thioredoxin-interacting protein-derived peptide (TN13) in macrophages.
  • To evaluate the efficacy of human immunodeficiency virus (HIV) trans-activator protein (TAT)-conjugated TN13 (TAT-TN13) in vitro and in vivo.
  • To elucidate the molecular mechanisms underlying the anti-inflammatory action of TAT-TN13.

Main Methods:

  • TAT-TN13 was synthesized and its cellular penetration into RAW 264.7 cells was confirmed.
  • The effect of TAT-TN13 on p38 MAPK activation was assessed in a dose-dependent manner.
  • Lipopolysaccharide (LPS)-induced expression of macrophage activation markers (CD80, CD86, MHC II) and transcription factors (NF-κB, AP-1) was measured.
  • Production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and mediators (NO, iNOS, COX-2) was quantified.

Main Results:

  • TAT-TN13 effectively penetrated RAW 264.7 cells and dose-dependently inhibited p38 MAPK activation.
  • TAT-TN13 significantly suppressed LPS-induced expression of CD80, CD86, MHC II, NF-κB, and AP-1.
  • TAT-TN13 markedly reduced the production of pro-inflammatory cytokines and mediators in vitro and in vivo.

Conclusions:

  • TAT-TN13 demonstrates potent anti-inflammatory activity in macrophages by inhibiting p38 MAPK signaling.
  • TAT-TN13 effectively suppresses key markers and mediators of macrophage activation.
  • TAT-TN13 represents a promising therapeutic candidate for treating inflammation-related diseases.
Keywords:
InflammationLPSMacrophageTN13TXNIPp38 MAPK

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