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Regulation of the Itaconate Shunt in ME/CFS

Regulation of the Itaconate Shunt in ME/CFS

Study Aim

This project aims to characterize the mitochondrial function in whole peripheral blood mononuclear cells (PBMCs) in ME/CFS.

Investigators

  • Robert Phair, PhD
  • Amanda Ooi, PhD
  • Ronald Davis, PhD

Updates and Potential

  • Our data demonstrates an abnormal mitochondrial function phenotype in ME/CFS cells, in which compromised cells fail to fulfill their own cellular energetic demands due to impaired TCA cycle in their cellular respiration.
  • There is also strong evidence for a pathogenic rewiring of mitochondrial central carbon metabolism in ME/CFS cells through the TCA cycle.
STUDY HYPOTHESIS AND DESCRIPTION

We are testing for a modification of mitochondrial central carbon metabolism, known as the itaconate shunt. The itaconate shunt is a 4-step pathway induced by infection or injury and the immune system’s response to that insult. A central tenet of this hypothesis is that ME/CFS is initiated when the itaconate shunt, normally a temporary response of the innate immune system, becomes a chronic impairment of the tricarboxylic acid cycle (TCA) in affected cells.

OBJECTIVES

Researchers wearing coats in modern research laboratory. Pc in laboratory.

  1. To assess and to characterize the mitochondrial function in whole PBMCs derived from healthy controls and ME/CFS patients.
  2. To test our hypothesis, i.e., the activation of the itaconate shunt and its role in rewiring the mitochondrial substrates from the TCA cycle into the itaconate metabolism pathway in ME/CFS cells.
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME / CFS) Post Treatment Lyme Disease Syndrome (PTLDS), Fibromyalgia Leading Research. Delivering Hope.Open Medicine Foundation®

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