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Hmm. I wonder if that has anything to do with the vaccine side effect blood clotting.
Hmm. Cytokines are chemical messengers. They are released to tell cells to self destruct when infected, as with covid (and other things). Which is the situation in covid infected lungs. Why do you think the ", postmortem examination of patients with COVID-19 has shown a large accumulation of inflammatory cells in lung tissues including macrophages and T-helper cells.(wikipedia)." Where else do you think the cytokines are coming from?
Theres a gunfight in a bar. Theres the gunmnen. Theres bullet holes. What do you think happened?
Cytokines do not tell cells to self-destruct in the general case (ignoring very specialised cells like mast cells and NK cells here)!!
Cytokines are a general warning signalling system. Part of the novelty of SARS-CoV-2 virus is that it effectively disables the interferon (cytokine) signalling early on in the COVID-19 disease.
Cell death is a very well regulated process, and for what should be obvious good reasons. There are many types of cell death - some are predetermined and orderly (apoptosis), some are traumatic/inflammatory/abrupt (necrosis).
There is a panoply of cell death phenotypes, including:
- Apopotosis is an ongoing cell death process provides for general cell turnover purposes,
- Autophagy removes damaged proteins and dysfunctional organelles by macrophage efferocytosis - mopping up of apoptotic cells and resolving inflammation,
- Necroptosis is an orderly form of necrosis, for when apoptosis signally is disrupted by a virus, and
- Pyroptosis, which occurs to rapidly clear infection but is signalled not by cytokines but by inflmmasones.
Inflammasones, together with pattern recognition receptors, detect pathogens and host-generated danger messages, to *regulate* cytokine release and cell death. [I think you might be mixing inflammasones and cytokines up?]
What happens in COVID-19 is that alveolar epithelial cells die by apopthosis/pyroptosis not because of cytokines but because of infection. This leads to macrophage activation, which causes pro-inflammatory cytokines to be released.
So, rather than cytokines being "released to tell cells to self destruct when infected", the dying infected cells are actually releasing cytokines which is then causing the inflammation. You had the cart before the horse.
In general, this cytokine release is a good thing. The problem is that with COVID-19 disease the release is too late and too excessive - the damage is mostly done. This combination of late and excessive cytokine release causes severe inflammation in the lungs, leading to a series of adverse outcomes (coronary atery disease, cardiomyopathy, coronary plaque microthrombogenesis), and also to dysfunctional hyper-coagulation.
Early clinical intervention with interferon (such as inhalation of IFN α-2b) may actually be associated with improved outcomes for COVID-19, allowing the immune system to better react earlier, without leading to the cytokine storm.
Interestingly, the cytokine storm is suspected to be one of the main causes of death in the Spanish 'flu also - and was worse with people with health immune systems because of their stronger immune response (and therefore higher increases in cytokine levels).
If you randomly toss a coin but each time its tails you discard that score...then you get an unending line of heads - the survivors.
You don't discard the score - it is evaluated. And the choice of which to discard is based on environmental conditions at the time. Most lineages blunder along an evolutionary path of speciation until they are either overly specialised or no longer adapted for the environment at the time and become extinct.