I just found a 1992 paper on some details of budesonide. If I understand it correctly, then budesonide has an effect on platelet aggregation of serotonin via the 5-HT2A receptor. (Which I haven’t learned to be common among steroids? But I’m a layman, so!)
The paper: Inhaled budesonide regimen enhances serotonin- and arachidonic acid-induced platelet aggregation – https://doi.org/10.1007/BF01991227
Platelet and serotonin interaction are intimately involved in inflammation and clotting. This interests me in connection with the randomized controlled trial study showing successful use of the SSRI fluvoxamine in managing severe COVID-19 cases, as defined by a measure of preventing clinical deterioration: https://doi.org/10.1001/jama.2020.22760
Also in relation with the quite sound-looking theory that the serotonin metabolism in the lung (a known aspect of the global serotonin mechanism) can be hit by the endothelial damage and inflammation in COVID-19, having the potential to cause a runaway feedback loop of inflammation and abnormal clotting. Platelets store serotonin, and serotonin is an immunomodulator, usually increasing inflammation in tissue, as well as usually causing veins and capillaries to contract. (As far as I understand things.) As yet unverified by a controlled trial, but there is a strong and clear theoretical basis and strong anecdotal indications. More info here: https://mobile.twitter.com/farid__jalali/status/133547064688...
CORRECTION:
The paper seems to indicate that budesonide has an effect of increasing the effect of serotonin to induce aggregation of blood platelets, theorized to happen via the 5-HT2A serotonin receptor.
CORRECTION: I must correct my lay hands’ pollution of the information on paper. The ‘92 study on budesonide makes an indicative argument towards action on the 5-HT2 receptor subtype. I mistakenly overspecified the 5-HT2A sub-subtype. I hope it isn’t grievously incorrect. There are three 5-HT2 receptor subtypes, A, B, and C: https://en.wikipedia.org/wiki/5-HT2_receptor – according to the individual Wikipedia entries, the 5-HT2A subtype is highly expressed on platelets, and the 5-HT2B is also expressed. No mention of platelets for the 5-HT2C subtype.
It is indeed true that psychedelics are generally known as agonists of the 5-HT2A receptor. Seemingly they tend to be agonists of the B and C subtypes as well, as per Wikipedia.
And interestingly enough, the substances known as psychedelics are also very significant and notable immunomodulators! As per this paper: Psychedelics and immunomodulation: novel approaches and therapeutic opportunities – A. Szabo, Frontiers of Immunology, 2015 – https://doi.org/10.3389/fimmu.2015.00358
(I want to mention author A. Szabo’s credentials: The 2015 paper cites the researcher’s position at Department of Immunology, Faculty of Medicine, University of Debrecen, Hungary. Subsequent publications show a position at the NORMENT Center of Excellence (CoE), Institute of Clinical Medicine, University of Oslo and the Department of Medical Genetics, both at Oslo University Hospital, Norway. Source: https://loop.frontiersin.org/people/193869/overview – There is reason to assume that this is a serious and capable person.)
There is mention of the Sigma-1 receptor as well in Szabo’s 2015 paper on immunomodulation. I want to take great care to not make spurious connections, but I did find this paper curious and interesting in this context: Repurposing Sigma-1 Receptor Ligands for COVID-19 Therapy? -
J. M. Vela, Frontiers of Immunology, November 2020 – https://www.frontiersin.org/articles/10.3389/fphar.2020.5823...
I just found a 1992 paper on some details of budesonide. If I understand it correctly, then budesonide has an effect on platelet aggregation of serotonin via the 5-HT2A receptor. (Which I haven’t learned to be common among steroids? But I’m a layman, so!)
The paper: Inhaled budesonide regimen enhances serotonin- and arachidonic acid-induced platelet aggregation – https://doi.org/10.1007/BF01991227
Platelet and serotonin interaction are intimately involved in inflammation and clotting. This interests me in connection with the randomized controlled trial study showing successful use of the SSRI fluvoxamine in managing severe COVID-19 cases, as defined by a measure of preventing clinical deterioration: https://doi.org/10.1001/jama.2020.22760
Also in relation with the quite sound-looking theory that the serotonin metabolism in the lung (a known aspect of the global serotonin mechanism) can be hit by the endothelial damage and inflammation in COVID-19, having the potential to cause a runaway feedback loop of inflammation and abnormal clotting. Platelets store serotonin, and serotonin is an immunomodulator, usually increasing inflammation in tissue, as well as usually causing veins and capillaries to contract. (As far as I understand things.) As yet unverified by a controlled trial, but there is a strong and clear theoretical basis and strong anecdotal indications. More info here: https://mobile.twitter.com/farid__jalali/status/133547064688...