Broderick, Fletcher, Klimas, Vernon, Taylor… this big NIH-funded study was loaded with top ME/CFS researchers. Similar to the Dubbo studies in Australia, the study followed people, in this case, adolescents, who came down with an infection (infectious mononucleosis), to see who would then come down with chronic fatigue syndrome and why.
Citing the many published studies linking ME/CFS onset to pathogens, the authors emphasized the strong link to infection found in this disorder.
“There remains…an overwhelming body of evidence reinforcing the link to an infectious etiology in at least a subset of CFS patients.”
Thus far the researchers have found that, by 6, 12 and 24 months after acute infectious mononucleosis, 13%, 7% and 4% of the adolescents met the criteria for chronic fatigue syndrome. Encouragingly, these are strikingly similar percentages to those found in other studies tracking infectious events.
Given the wide range of documented ME/CFS pathogen triggers (EBV, Cytomegalovirus, HHV-6, Q-fever, Ross-River Virus, enterovirus, parvovirus B-19, giardia) it’s probably time to wonder if a subset of people infected by ANY serious pathogen might not be left with ME/CFS for a significant period of time.
If that’s true then this disorder may be far more common than anyone has suggested yet.
In this study the researchers examined 16 immune factors called cytokines using the latest methods, and gave their analysis a twist: Since cytokines usually co-occur together, they looked at 'combinational effects' to see if suites of cytokines showed up together.
Results
First they found IL-8 was increased and IL-23 was decreased in people with post-infectious CFS. Then, using a more sophisticated analysis they found that they could predict 80% of the people who came down with ME/CFS simply by examining the levels of 5 cytokines (IL-2, IL-6, IL-8, IL-23 and IFN-y) in their blood.
Focus on IL-8
Il-8 has all sorts of interesting potential tie-ins with ME/CFS.
We know the sympathetic nervous system (fight or flight response) is over-activated in this disorder and IL-8 has been linked to sympathetic nervous system induced pain, as well as pain in fibromyalgia, and is up-regulated in a key brain region (the anterior cingulate cortex (ACC)) believed to play a role in both chronic fatigue syndrome and FM.
IL-8 is also produced by cells with toll-like receptors that participate in the early, innate immune response, which has been showing up in spades in CFS research recently.
The fact that these researchers were able to pick out 35 of the 42 ME/CFS patients simply by measuring five cytokines demonstrated that the group was in the grip of a substantial immune dysregulation.
Pathogen Fighting System May Be Blunted in Adolescents with CFS
But what
kind of immune dysregulation? Four of the five cytokines highlighted in the study play a role in the Th17 system, an important player in the fight against opportunistic infections and a known culprit in auto-immune diseases and inflammation.
This study suggested that a poorly functioning TH17 pathway could be preventing these young ME/CFS patients from clearing EBV from their systems. Interestingly, some studies suggest EBV may be able to modify the TH17 system, thus clearing the way for greater infectiveness.
Whom Do These Findings Apply To?
The authors noted that these findings could apply to patients with other types of infectious onset, or they could be peculiar to this group.
In a previous study involving a more general population of ME/CFS patients, the researchers found lower IL-8 levels, instead of the higher levels found in the present study. The contrast in findings of the two studies outlines the high level of heterogeneity in the ME/CFS community - and the urgent need to develop subsets.
