Cytokine network analysis in a community-based pediatric sample of patients with myalgic encephalomyelitis/chronic fatigue syndrome, 2022, Jason et al

[Sly Saint]

Abstract
Objectives: Studies have demonstrated immune dysfunction in adolescents with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS); however, evidence is varied. The current study used network analysis to examine relationships between cytokines among a sample of pediatric participants with ME/CFS.

Methods: 10,119 youth aged 5-17 in the Chicagoland area were screened for ME/CFS; 111 subjects and controls were brought in for a physician examination and completed a blood draw. Youth were classified as controls (Cs, N = 43), ME/CFS (N = 23) or severe (S-ME/CFS, N = 45). Patterns of plasma cytokine networks were analyzed.

Results: All participant groups displayed a primary network of interconnected cytokines. In the ME/CFS group, inflammatory cytokines IL-12p70, IL-17A, and IFN-γ were connected and included in the primary membership, suggesting activation of inflammatory mechanisms. The S-ME/CFS group demonstrated a strong relationship between IL-17A and IL-23, a connection associated with chronic inflammation. The relationships of IL-6 and IL-8 in ME/CFS and S-ME/CFS participants also differed from Cs. Together, these results indicate pro-inflammatory responses in our illness populations.

Discussion: Our data imply biological differences between our three participant groups, with ME/CFS and S-ME/CFS participants demonstrating an inflammatory profile. Examining co-expression of cytokines may aid in the identification of a biomarker for pediatric ME/CFS.

https://pubmed.ncbi.nlm.nih.gov/35570777/

 

[cfsandmore]

Will this possible bio marker work for adults?

 

[Jonathan Edwards]

I cannot see any biomarker here. They report some correlations within groups but say nothing about differences between groups in the abstract.

 

[Hutan]

but say nothing about differences between groups in the abstract.

Yes, the abstract isn't very helpful, and, at the moment, the abstract is all there is. The paper is labelled 'online ahead of print'.

If the definition of ME/CFS and severe ME/CFS is consistent with another recent paper by Leonard Jason, then 'severe ME/CFS' refers to compliance with multiple main ME/CFS criteria.

The S-ME/CFS group demonstrated a strong relationship between IL-17A and IL-23, a connection associated with chronic inflammation.

I find this interesting, even though we don't yet know if it is actually different to the situation in controls. If it's a real difference, perhaps it is an important clue.

See for example this paper, where relationships between IL-23 and IL-17 seem to create a 'self-amplifying... inflammatory response'
Discovery of the IL-23/IL-17 Signaling Pathway and the Treatment of Psoriasis
2018

Psoriasis vulgaris is a common, heterogeneous, chronic inflammatory skin disease characterized by thickened, red, scaly plaques and systemic inflammation. Psoriasis is also associated with multiple comorbid conditions, such as joint destruction, cardiovascular disease, stroke, hypertension, metabolic syndrome, and chronic kidney disease. The discovery of interleukin-17-producing T helper cells in a mouse model of autoimmunity transformed our understanding of inflammation driven by T lymphocytes and the subsequent development of disease like psoriasis. Under the regulation of interleukin-23, T cells that produce high levels of interleukin-17 create a self-amplifying, feed-forward inflammatory response in keratinocytes that drives the development of thickened skin lesions infiltrated with a mixture of inflammatory cell populations. Recently, the FDA approved multiple highly effective psoriasis therapies that disrupt interleukin-17 (secukinumab, ixekizumab, and brodalumab) and interleukin-23 (guselkumab and tildrakizumab) signaling in the skin, thus leading to a major paradigm shift in the way that psoriatic disease is managed.