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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Opiates promote T cell apoptosis through JNK and caspase pathway

P Singhal1, A Kapasi, K Reddy

  • 1Division of Kidney Diseases and Hypertension, Long Island Jewish Medical Center, New Hyde Park, NY 11040, USA.

Advances in Experimental Medicine and Biology
|December 1, 2001
PubMed

Insights

Opiate use triggers T cell death by activating specific molecular pathways. This research reveals how morphine and related compounds induce apoptosis, impacting immune function in addicts.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Opiate addiction is linked to increased susceptibility to infections.
  • The precise molecular mechanisms underlying opiate-induced immune dysfunction require further elucidation.

Purpose of the Study:

  • To investigate the molecular pathways responsible for opiate-induced T cell apoptosis.
  • To identify key signaling molecules and enzymes involved in this process.

Main Methods:

  • T cells were treated with morphine and DAGO ([D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin).
  • Apoptosis, kinase activation (JNK, MAPK, ERK), and caspase activity were assessed.
  • Expression levels of ATF-2 and cleavage of PARP were analyzed.

Main Results:

  • Morphine and DAGO significantly enhanced T cell apoptosis.
  • Opiates activated c-Jun NH2-terminal kinase (JNK) and increased ATF-2 expression.
  • Opiates attenuated extracellular signal related kinase (ERK) and induced cleavage of caspases 8, 9, 10, and PARP, indicating caspase-3 activation.

Conclusions:

  • Opiate-induced T cell apoptosis is mediated by the JNK signaling cascade.
  • Activation of caspases 8 and 3 plays a critical role in opiate-driven T cell death.

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