Covid-19 induces proinflammatory cytokine signals Reader 05/01/2020 (Fri) 21:28:58 Id: eb148b No.15854 del
More information on Covid-19. It does not directly attack the lungs as is thought by the mainstream. Lungs are weakened due to cerebral infection. Covid-19 attacks the brain as a neurotoxin and can cause severe unnatural cerebral responses.
https://www.qeios.com/read/FXGQSB
http://archive.is/9PjcJ
>neurological/psychiatric disorders, especially loss of sense of smell which is specific of the disease
>systemic hyperinflammatory syndrome with increased levels of circulating cytokines and atypical acute respiratory distress syndrome with loss of neurological control of lung perfusion regulation and hypoxic vasoconstriction
>ACE2 is expressed at the transcriptomic level in the lung, the small intestine and colon, in the kidney, in the testis, in the heart muscle and in the brain, yet the protein is not detected in the lung
>In the brain, ACE2 is expressed in both neurons and glia and particularly present in the brain stem and in the regions responsible for the regulation of cardiovascular functions, including the subfornical organ, paraventricular nucleus, nucleus of the tractus solitarius, and rostral ventrolateral medulla
>There is strong evidence for a neurotropic action of SARS-CoV-2 infection. It has been demonstrated that β-coronaviruses to which the SARS- CoV-2 belongs, do not limit their presence to the respiratory tract and have been shown to frequently invade the CNS (central nervous system)
>Neuroinfection has been proposed to potentially contribute to the pathophysiology and clinical manifestations of Covid-19 with the neuroinvasive potential of SARS-CoV-2 suggested to play a role in the respiratory failure of Covid‐19 patients
>More recently, a study of 214 Covid‐19 patients further found that about 88% (78/88) of the severe patients displayed neurologic manifestations including acute cerebrovascular diseases and impaired consciousness.
>the nicotinic acetylcholine receptor (nAChR) plays a key role in the pathophysiology of Covid-19 infection and might represent a target for the prevention and control of Covid-19 infection.
>Based on an epidemiological survey on Covid‐19, the median time from the first symptom to dyspnea was 5.0 days, to hospital admission was 7.0 days, and to the intensive care was 8.0 days
>The nAChR pathway is hypothesized to be engaged in the Covid-19 inflammatory syndrome. The nervous system, through the vagus nerve, can significantly and rapidly inhibit the release of macrophage TNF, and attenuate systemic inflammatory responses
>This cytokine profile shows striking analogies with the cytokine storm syndrome, leading to the hyperinflammatory syndrome described in a subgroup of Covid-19 patients
>Interestingly, 𝛼7 agonists, including nicotine, have proven to be effective in reducing macrophage cytokine production and inflammation in animal models of pancreatitis and peritonitis
>In this setting, a nicotinic treatment that might possibly antagonize the blocking action of SARS-CoV-2 on the AChR through a possible modulation of the ACE2 – nAChR interaction, would act earlier than anti-cytokine therapies.
>nAChR modulation by Covid-19 might tentatively account for the hyperinflammatory features observed in a subgroup of Covid-19 patients, mimicking bona fide the macrophage activation syndrome.

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