Reductions in circulating levels of IL-16, IL-7 and VEGF-A in ME

[natasa778]

Cytokine. 2015 Nov 23;78:27-36. doi: 10.1016/j.cyto.2015.11.018. [Epub ahead of print]
Reductions in circulating levels of IL-16, IL-7 and VEGF-A in myalgic encephalomyelitis/chronic fatigue syndrome.
Landi A1, Broadhurst D2, Vernon SD3, Tyrrell DL4, Houghton M5.
Author information
Abstract
Recently, differences in the levels of various chemokines and cytokines were reported in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) as compared with controls. Moreover, the analyte profile differed between chronic ME/CFS patients of long duration versus patients with disease of less than 3years. In the current study, we measured the plasma levels of 34 cytokines, chemokines and growth factors in 100 chronic ME/CFS patients of long duration and in 79 gender and age-matched controls. We observed highly significant reductions in the concentration of circulating interleukin (IL)-16, IL-7, and Vascular Endothelial Growth Factor A (VEGF-A) in ME/CFS patients. All three biomarkers were significantly correlated in a multivariate cluster analysis. In addition, we identified significant reductions in the concentrations of fractalkine (CX3CL1) and monokine-induced-by-IFN-γ (MIG; CXCL9) along with increases in the concentrations of eotaxin 2 (CCL24) in ME/CFS patients. Our data recapitulates previous data from another USA ME/CFS cohort in which circulating levels of IL-7 were reduced. Also, a reduced level of VEGF-A was reported previously in sera of patients with Gulf War Illness as well as in cerebral spinal fluid samples from a different cohort of USA ME/CFS patients. To our knowledge, we are the first to test for levels of IL-16 in ME/CFS patients. In combination with previous data, our work suggests that the clustered reduction of IL-7, IL-16 and VEGF-A may have physiological relevance to ME/CFS disease. This profile is ME/CFS-specific since measurement of the same analytes present in chronic infectious and autoimmune liver diseases, where persistent fatigue is also a major symptom, failed to demonstrate the same changes. Further studies of other ME/CFS and overlapping disease cohorts are warranted in future.

http://www.ncbi.nlm.nih.gov/pubmed/26615570

 

[Jon_Tradicionali]

Associations come in the dozens. However these are all downstream factors which make it impossible to connect the dots without looking further upstream as to the causative agent.

 

[Gijs]

I get a little tired of all those cytokines studies. Cytokines are complicated in ME/CFS. It will never lead to a specific biomarker in this disease.

 

[msf]

My VEGF (as measured by Redlabs) was half the lowest normal value.

 

[MikeJackmin]

Associations come in the dozens. However these are all downstream factors which make it impossible to connect the dots without looking further upstream as to the causative agent.

This is a bit more interesting that usual:

>This profile is ME/CFS-specific since measurement of the same analytes present in chronic infectious and autoimmune liver diseases, where persistent fatigue is also a major symptom, failed to demonstrate the same changes.

If further studies bear this out we might have a useful biomarker after all.

 

[halcyon]

I'm curious why we seem to have so much eosinophil recruitment going on, found both here and in the Columbia CSF study.

 

[alex3619]

100 chronic ME/CFS patients of long duration

I just wanted to emphasize this part. This is the first independent use of the long-term/short-term cytokine shift in ME/CFS patients.

We had so many problematic studies because, as it appears with current science, there are different subgroups ... and not because they have something different wrong with them. Severity and disease duration both change the cytokine pattern. If you lump people with different severity or different disease progression you may get a result mishmash. So in a bunch of studies the results might be all over the place.

We already have many biomarkers. The problem is in going from biomarker to demonstrated diagnostic biomarker. This is not a trivial process, and requires more expensive studies ... and when has there ever been much money?

 

[Research 1st]

This appears to be another study from pro government CFS researchers apparently referring to the 'ME/CFS (whatever that is) ,but when you know the science, turns out to be the opposite of ME l

Actual ME clinicians.

Dr De Meirleir
Dr Montoya
Dr Cheney
Dr Peterson

All see ME sufferers in USA, Europe.

They know ME is associated to elevated cytokines. De Meirleir (at the very least) will also tell you some ME sufferers have elevated VEGF. I'll tell you why, as it's associated to intracellular infections ,such as Bartonella.

So the idea that the Vernon paper is saying there diminished VEGF could be a biomarker is dubious in terms of legitimacy for 'ME', for example, myself and others have tested their VEGF and......ours are very high.

I have ME, as I have the damage ME causes:

POTS, Autonomic Neuropathy, Trigeminal Neuralgia, Arthritis, Asthma, Multiple Allergies, Osteoporosis,Multiple vitamin and co factor deficiencies. NB: Notice none of my 'abnormal findings' involves 'Self Reported Unexplained Chronic Fatigue', it involves syndromes and damage, by having an uncontrolled disease state, possibly autoimmume, or untreated infection which is explained.

The damage found in ME, is explained. Hence ME can never be CFS and hence ME/CFS research can never, legitimately, be associated to ME, as with CFS, the 'fatigue' must be unexplained, and no damage to the body can be allowed to be present. NB: Not my rules, the CDC's rules.

I'm not unique there are millions of others out there with
my immune profile, who are severely affected who have very high Cytokines, VEGF and everything else Lipkin and CDC allied researchers can't find.

Now isn't that a strange happening, as it shows, that ME sufferers are excluded from research, because of the diagnostic criteria, the excludes people with active signs of disease and explained reasons for Chronic Fatigue.

And for ME research, that is very bad, and it means these papers get churned out, with people presuming that chronically fatigued patients, represent ME sufferers biologically. Nope, they don't.

It irritates me, researchers title their papers ME/CFS, or CFS/ME,without thinking of the damage they unintentionally can do to PWME who do have high cytokines, VEGF, Interferon Gamma etc, decades after diagnosis and that is part of the reason they are housebound, severely affected etc.

 

[msf]

I and quite a few other KDM patients have low VEGF, so I don´t think he would be that surprised by this finding (I know more KDM patients without a Bartonella infection than with one). I think he would be more surprised by the IL-7 finding, since his cytokine study found that this was upregulated, as, the paper pointed out, is common in inflammatory/autoimmune diseases such as RA. Of course, it could be upregulated in the short duration patients, and downregulated in the long duration ones, and still show an overall upregulation.

I think it is likely that there will be some ´immune exhaustion´ in some patients, since, as the Lipkin study mentioned, this is also found in HCV infection, and I believe that ME is the result of a chronic infection.

 

[CFS_for_19_years]

Full article attached here.

 

[out2lunch]

My VEGF is midrange normal, but my IL-7 is very low. In fact, out of the nine interleukins I've had measured, only one was off the chart, 20 times above normal (IL-9).

I keep reading about ME/CFS patients having inflammatory/autoimmune conditions and elevated interleukins. I've had both Hashi's and Guillain-Barre, but have never quite fit the model seen in so many other autoimmune patients.

Perhaps the immune shift for long-term patients such as myself (26 years and counting) is where the focus should be. Maybe ME/CFS becomes an entirely different disease after a significant passage of time.