Study links ME/CFS immune-cell defect to impaired energy production
Griffith University researchers say faulty calcium flow into mitochondria in immune cells may help explain low energy and immune dysfunction in ME/CFS.
By Priya Raghavan · Science Reporter
2 min read
Griffith University researchers have reported an immune-cell abnormality in people with myalgic encephalomyelitis/chronic fatigue syndrome that may help explain the severe lack of energy associated with the illness. The team said the finding points to a possible biological chain from faulty ion-channel activity to reduced mitochondrial function.
The research, published in BMC Immunology, examined calcium movement linked to TRPM3, an ion channel previously studied by Griffith’s National Center for Neuroimmunology and Emerging Diseases. The paper is titled “Deficient TRPM3-linked mitochondrial Ca2+ influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome.”
Lead author Chandi Magawa, a Ph.D. candidate at Griffith, and colleagues used live-cell imaging to watch TRPM3-dependent calcium movement into mitochondria in natural killer cells. According to Griffith University, the work was designed to test whether mitochondrial deficits reported by other researchers could be a consequence of earlier identified ion-channel and calcium abnormalities.
Magawa said the team found a significant dysfunction in the TRPM3-calcium pathway in ME/CFS. She said that dysfunction was associated with reduced calcium entry into mitochondria, the part of the cell involved in energy production.
According to Magawa, lower calcium movement into mitochondria could weaken immune-cell function and energy production, setting off broader effects in the body. The study focused on natural killer cells, a type of immune cell, and did not report a cure or treatment.
What the study adds
Griffith University said the findings build on earlier work pointing to ion-channel and calcium-signaling problems in ME/CFS. By connecting those abnormalities to mitochondrial calcium uptake, the researchers said the study offers a possible explanation for how cellular signaling defects could contribute to energy problems.
Dr. Natalie Eaton-Fitch said ME/CFS is a serious and complex illness with no cure or treatment. Citing the Australian Institute of Health and Welfare, she said an estimated 219,000 Australians are living with the condition.
Eaton-Fitch said symptoms can include severe ongoing exhaustion, post-exertional malaise, pain, cognitive problems, dizziness, temperature instability and sensitivity to sensory input. She said those symptoms can sharply limit daily activities, education, employment and social participation.
Professor Sonya Marshall-Gradisnik, director of Griffith’s National Center for Neuroimmunology and Emerging Diseases, said the study helps clarify biological dysfunction in ME/CFS. She said the work could contribute to future diagnostic biomarkers and therapies aimed at ion-channel dysfunction or calcium signaling.
The findings do not establish a clinical test or approved therapy. Griffith University presented the research as a step toward understanding mechanisms that may underlie ME/CFS symptoms and immune-cell dysfunction.
This story draws on original reporting from Medical Xpress.