Science always tries to build on prior knowledge. Understanding how COIVID 19 creates such inflammation means evaluating whether this coronavirus mimics cytokine storm diseases which we already know, or stirs up different immune winds of its own. We have some experience and some therapies for some diseases called auto-inflammatory conditions and scientists wonder if those therapies might work for COVID 19’s inflammation. These researchers would assert that the differences are too great after studying which cytokines and immune biomarkers were different with COVID 19.
Auto-inflammatory conditions are rather rare diseases which the public would usually not recognize. Scientists compared the known cytokine levels form two of these diseases, macrophage activation syndrome (MAS) and secondary hemophagocytic lympohistiocytosis (sHHLH). In MAS, macrophages, immune cells which eat microbial invaders, become constantly over activated leading to unnecessary ongoing inflammation. The cytokines, or immune messengers, that they release trigger other inflammation and thus symptoms.
The sHLH condition occurs when a type of lymphocyte, immune cells subtype, called a histiocyte, continues on an eating rampage, chomping on your red blood cells. This leads to anemia and once again, unchecked inflammation. Neither condition is fun to experience.
COVID 19 came along and in some patients triggers extreme inflammation. This extreme inflammation can lead to death or at least major short- and long-term damage. Given the mixed responses to various anti-cytokine therapies and these symptoms, the term ‘cytokine storm’ caught the public’s attention.
By comparing MAS and sHLH to COVID 19’s measured levels of 22 different markers, the patterns “clearly separate” the former two from the latter infection. Levels of interleukin 18, interferon gamma, interleukin 1 receptor antagonist, intracellular adhesion molecule 1, interleukin 8, and soluble Fas ligand were considerably divergent between them. While COVID 19 clearly triggers extreme levels of inflammation, the mechanisms by which it increases inflammation are not simple copies of these auto-inflammatory conditions. Therefore the therapies designed for the former two are not as hopeful options for the latter.
As we work towards understanding COVID 19 in 2021 and beyond, we must build on prior knowledge but not get trapped in our thinking paths based on superficial similarities. Our body systems are far too intricate and complex to base life and death decisions on surface commonalities. Real science requires some digging into the deep recesses of the inter-workings of our immune system if we hope to combat new diseases like COVID 19. Meanwhile, we in functional medicine can utilize some natural therapies which modulate and dampen multiple immune mechanisms without completely shutting them off like many pharmaceuticals do.
Christoph Kessel, Richard Vollenberg, Katja Masjosthusmann, Claas Hinze, Helmut Wittkowski, France Debaugnies, Carole Nagant, Francis Corazza, Frédéric Vély, Gilles Kaplanski, Charlotte Girard‐Guyonvarc’h, Cem Gabay, Hartmut Schmidt, Dirk Foell, Phil‐Robin Tepasse. Discrimination of COVID‐19 from inflammation‐induced cytokine storm syndromes by disease‐related blood biomarkers. Arthritis & Rheumatology, April 20, 2021; DOI: 10.1002/art.41763
Thanks to Science Daily:
Wiley. “New insights on inflammation in COVID-19.” ScienceDaily. ScienceDaily, 21 April 2021. <www.sciencedaily.com/releases/2021/04/210421082906.htm>.