There is a long thread here called "There are markers of inflammation being found in fibro". It has 30-35 studies summarized & also with links. Use the search box and looking for "fibro inflammation."
I'm also linking to Fibromyalgia study finding more 2 inflammatory cytokines : TNF & Interleukin-6/IL-6 & 1 other thing, HK, that I'm not yet familiar with, in blood serum. This is from Tufts, by a Theoharides team. Substance P was there, too. As I've said, its a mast celll trigger.
-- (IL-6 an inflammatory cytokine, can also initiate the "acute phase" immune response.)
-- Calling CRH a "neuropeptide" is new to me. It's also a stress hormone, the first to be released under stress, from the hypothalamus. And it asks the pituitary to ask the adrenals for cortisol (cortisol is antiinflammatory, you might say its the original prednisone) CRH triggers mast cells.
Title: Neuropeptides CRH SP, HK-1, and Inflammatory Cytokines: IL-6 and TNF, Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells
J. Pharmacol. Exp. Ther.
Irene Tsilioni et al (with Theoharides)
jpet.aspetjournals.org/content/356/3/664.abstract----- -----
I might be the only one here interested in Vascular Endothelial Growth Factor/VEGF.
I think Sturgill's team was the only one that ever looked for IL-33 in fibro patients...I don't think I ever dug thru any tables they might have had. I dont think it was elevated in Sturgill et al but idk for sure. Their goal was really determining which Th (T helper) immune system was dominant, and I think what they did was set a thresh hold for taking cytokines into consideration.
Study title (not a fibro or ME/CFS study):
Vascular endothelial growth factor (VEGF), mast cells and inflammation.
"Substance P strongly induces VEGF in mast cells, and IL-33 contributes to the stimulation and release of VEGF in human mast cells in a dose-dependent manner and acts synergistically in combination with Substance P. Here we report a strong link between VEGF and mast cells and we depict their role in inflammation and immunity."
www.ncbi.nlm.nih.gov/pubmed/23755748A fibro study found that Substance P/SP in cerebral spinal fluid is higher, also same finding in a fibro muscle study. SP is in plenty of places.
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The second gene expression study of the year was recently published. Get past the study & I have some summary for you.
"Our hypothesis is that there is an upregulation of immune/inflammatory molecules in the blood of FM patients with a concomitant decrease in pathways related to hypersensitivity and the allergic responses." The authors
Fibromyalgia patients exhibited a differential expression of 421 genes, several relevant to pathways for pain processing, such as glutamine/glutamate signaling and axonal development.
There was also an upregulation of several inflammatory pathways and downregulation of pathways related to hypersensitivity and allergy. Using rigorous diagnostic modeling strategies, we show “locked” gene signatures discovered on Training and Test cohorts, that have a mean Area Under the Curve (AUC) of 0.81 on randomised, independent external data cohorts.
Lastly, we identified a subset of 10 probesets that provided a diagnostic sensitivity for FM of 95% and a specificity of 96%. We also show that the signatures for FM were very specific to FM rather than common FM comorbidities.
Publ. in Clin Exp. of Rheum. May-June 2016
www.ncbi.nlm.nih.gov/pmc/articles/PMC4888802/
Cort Johnson at HealthRising wrote:
That was intriguing given that the expression of genes associated with granulocytes (mast cells, neutrophils, eosinophils, basophils) was reduced in the FM patients. These granule containing immune cells are associated with mast cell activation and the allergic response. Some researchers believe they may also be tweaking the nerves and contributing to pain sensitization.
Does the reduced expression of allergic genes mean FM is an inflammatory disease which results in a reduced mast cell activation syndrome? Apparently the authors don't believe so. The evidence in FM trends towards mast cell activation not the opposite, and the authors emphasized three studies which have found an overexpression of mast cells in the skin of FM patients. One of the genes (CPA3) highlighted - a biomarker for local and systemic mast cell degranulation - suggested that mast cell activation (MCA) had occurred. [Mast cells release inflammatory cytokines and many other problematic mediators.]
They found 428 significantly differentially expressed genes in FM and focused on the top twenty. A genetic network analysis found a trend towards an increased inflammatory response with the most significant group of genes associated with allergy and hypersensitivity. The inflammatory hub was centered on the IL-10 gene - a anti-inflammatory cytokine that has been highlighted in chronic fatigue syndrome several times. High IL-10 levels have been associated with attempts to turn down an overactive immune response.
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I wonder if it's also a matter of being unable to put out enuf Interleukin 10 to compensate. (IL-10 is an anti-inflammatory cytokine.) Professor Linda Watkins' strategy to fight neuroinflammation is to gain more IL-10. She says in a youtube interview that this was successul in neuropathic pain in dogs, and now her team should be doing her MS study. I hope it has begun by now.
Post Edited (Rockon) : 12/20/2016 1:23:16 AM (GMT-7)