It's too late, I'm deeply, deeply offended. And I simply don't understand your reticence to share private health information with strangers on the internet. /s
Ok, so from what I understand, much of the fallout from a coronavirus infection in severe cases is resulting from an overreaction by the immune system. What I saw in the original paper you shared is that the most plausible mechanism would be increased propensity for isolation and mask wearing, but the IL-6 knockdown would be through CF deactivating elements of the immune system (immune signaling molecules).
The Nature paper suggests upregulation of inflammation, which seems implausible to me: "Activation of furin, which is increased in CF, together with the cellular damage induced by viroporins, might be expected to upregulate NLRP3 and cause inflammation"
The proposed mechanism in the Physio paper is as follows: "Our analysis revealed that ACE2 mRNA is elevated and TMPRSS2 mRNA is decreased in CF airway epithelial cells compared with non-CF cells. Increased ACE2 is predicted to enhance SARS-CoV-2 binding to epithelial cells but would increase conversion of ANG II, which is proinflammatory, to angiotensin-1–7, which is anti-inflammatory. Thus, increased ACE2 would reduce inflammation and lung damage due to SARS-CoV-2. Moreover, decreased TMPRSS2 would reduce SARS-CoV-2 entry into airway epithelial cells"
So, again, there isn't hard evidence that this is happening at all, but here are a couple of proposed mechanisms that could potentially explain it if it is happening.
I'm not qualified to continue this discussion. I have no idea what in heck furins are. I'm just a former homemaker with the rude habit of failing to keel over dead from my condition. I don't speak medicalese.
Ok, so from what I understand, much of the fallout from a coronavirus infection in severe cases is resulting from an overreaction by the immune system. What I saw in the original paper you shared is that the most plausible mechanism would be increased propensity for isolation and mask wearing, but the IL-6 knockdown would be through CF deactivating elements of the immune system (immune signaling molecules).
The Nature paper suggests upregulation of inflammation, which seems implausible to me: "Activation of furin, which is increased in CF, together with the cellular damage induced by viroporins, might be expected to upregulate NLRP3 and cause inflammation"
The proposed mechanism in the Physio paper is as follows: "Our analysis revealed that ACE2 mRNA is elevated and TMPRSS2 mRNA is decreased in CF airway epithelial cells compared with non-CF cells. Increased ACE2 is predicted to enhance SARS-CoV-2 binding to epithelial cells but would increase conversion of ANG II, which is proinflammatory, to angiotensin-1–7, which is anti-inflammatory. Thus, increased ACE2 would reduce inflammation and lung damage due to SARS-CoV-2. Moreover, decreased TMPRSS2 would reduce SARS-CoV-2 entry into airway epithelial cells"
So, again, there isn't hard evidence that this is happening at all, but here are a couple of proposed mechanisms that could potentially explain it if it is happening.
Also I skimmed these things, so grain of salt.