Aspects of the Jarisch-Herxheimer reaction can resemble opiate withdrawal. What would it look like clinically if there was a pro-inflammatory cytokine(s) or biotoxin that competitively bound to endorphin or enkephalin receptors causing a patient to "withdraw" from their own endogenous opiates? Does this have any relevance in understanding fibromyalgia, or other pain syndromes?
Dear Dr Shepler,
From structurally point of view, enkephalin receptors such as the opioid receptor OPRM1 are 7_tm receptors, as other known GPCRs such as CXCR- and CCR-. So OPRM1 could bind specific ligands as IL-8 (that physiologically binds CXCR1/2). Moreover, algorithms such as Springdb predict interactions between CXCR2 and OPRM1, demonstrating that maybe a mutual cooperation among these receptors (and perhaps a crosstalk between the immune system and the opiate withdrawal ) occurs. Specifically I cannot answer to questions upon relevances of this hypothesis in fibriomyalgia or other pain syndromes, but If I have understood your question, I think that you should find useful this recent paper: "Opioid and chemokine receptor crosstalk: a promising target for pain therapy?" published by Stéphane Mélik Parsadaniantz:
http://www.nature.com/nrn/journal/v16/n2/abs/nrn3858.html
In attachment, the paper.
Thanks for your interesting question
Luca
Article Cytokines play an aetiopathogenetic role in fibromyalgia: A ...
https://www.ncbi.nlm.nih.gov/books/NBK470156/
https://www.ncbi.nlm.nih.gov/pubmed/26088214
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