Update on Solve ME/CFS 2017 Funding - Prof Bergquist

bertiedog

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I had this brief update sent through today by email and wasn't sure if their work had been discussed here. It looks very interesting to my rather unscientific eyes!

Sailing Ahead: Interim Update from 2017 Ramsay Class Member Prof. Jonas Bergquist
Reporting from a tall-ship cruiser, Prof. Bergquist (Uppsala University) tells us a bit more about the Ramsay-supported study he is navigating along with his co-Investigator Prof. Jonas Blomberg. The project is anticipated to wrap up at the end of this year.

Prof. Jonas Bergquist teamed up with Prof. Jonas Blomberg at Uppsala University and the Gottfries Clinic in Sweden to investigate an autoimmunity pathogenesis (onset and development) of ME/CFS. The researchers are looking to build on evidence from past studies of a possible link between infection-triggered ME/CFS and metabolic dysfunction. As part of this Ramsay project, Prof. Blomberg published the explanatory disease model motivating this research in Frontiers in Immunology.

Prof. Blomberg has already used serology (analyzing antibodies in blood) to look for indications of past infections in patients and the presence of autoantibodies (antibodies produced by the immune system that mistakenly target a person’s own tissues). For his part of the project, Prof. Bergquist has developed a method for in-depth screening of disturbances in the thyroid hormone regulation in ME/CFS patients. Thyroid hormones are involved in numerous physiological processes, including metabolic processes and immune function. Read the study abstract for their Ramsay project here and stay tuned for future updates.

Pam
 

Cort

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I'm very impressed with Bergquist and Blomber and am glad the SMCI are funding them

You can find a blog on Blomberg's model at the Simmaron Research Foundation. It involves a really interesting gut hypothesis

http://simmaronresearch.com/2018/09/autoimmune-model-chronic-fatigue-syndrome-begins-gut/

Blomberg proposes that the breach of your gut barrier created a state of low level chronic inflammation prior to you getting ME/CFS. The gut barrier is important because it’s a place in the body where tolerance (the ability to distinguish between self and non-self antigens) is more difficult to maintain. Given the extraordinary diversity and sheer number of gut bacteria, it’s easy to see how the immune system could be overwhelmed and lose it’s way.

Blomberg believes that slow leakage from the gut created a population of auto-reactive B-cells that remained mostly inactive or quiescent (in a state of anergy), almost like undercover agents infiltrating a city, waiting for the signal to pounce. At some point a “decisive” immune event flipped them into action, and an autoimmune disease – ME/CFS – was born.

He bases his hypothesis of pathogenic autoantibody creation in ME/CFS on a process that appears to be occurring in lupus. The first step occurs when a genetically predisposed person meets up with bad gut bacteria. First, abnormal but not pathogenic B-cells, which have a “weak autospecificity”, appear. These weakly targeted B-cells are not strongly directed against a specific antigen or part of the cell and don’t appear to be particularly dangerous at first, but the body should still eliminate them. Blomberg proposes that it doesn’t.

Over time exposure to the bad gut bacteria causes the specificity of the B-cells to change – making them more targeted and dangerous. At some point an infection turns them on and they start producing clones of themselves which begin attacking the body. ME/CFS is born.