LLight
Member
- Joined
- May 30, 2018
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- 1,411
A recent preprint on COVID19 is saying that:
If I'm reading this well and that their observations are conclusive, it's M2 macrophages that are involved in the worst cases of COVID19.
Interestingly, the transcription factor NFAT5 which is supposedly increased by dehydration and probably fasting too (also called TonEBP in the literature) tends to suppress the HO-1 enzyme in macrophages.
Moreover, the HO-1 enzyme favor the M2 polarization of macrophages (from the same publication):
"Of particular note, we found the alveolar macrophages with SARS-CoV–2 infection were expressing ACE2, a well-established receptor for both SARS-CoV and SARS-CoV–2 (Extended Data Fig.5). It was reported that SARS-CoV could occasionally be identified in the alveolar macrophages. In COVID–19
patients, the extraordinary aggregation and activation of these macrophages could occupy a central position in pathogenesis of the very severe “inflammatory factor storm” or “cytokine storm”.
Therefore, the spectacular infiltration and activation of alveolar macrophages in COVID–19, especially among patients with severe and critical stages of ARDS, might represent the shift of classically activated phenotype (M1) to alternatively activated phenotype (M2) of alveolar macrophages, whereas this shifted property of alveolar macrophages could contribute to the inflammatory injuries and fibrosis of respiratory tracts."
patients, the extraordinary aggregation and activation of these macrophages could occupy a central position in pathogenesis of the very severe “inflammatory factor storm” or “cytokine storm”.
Therefore, the spectacular infiltration and activation of alveolar macrophages in COVID–19, especially among patients with severe and critical stages of ARDS, might represent the shift of classically activated phenotype (M1) to alternatively activated phenotype (M2) of alveolar macrophages, whereas this shifted property of alveolar macrophages could contribute to the inflammatory injuries and fibrosis of respiratory tracts."
If I'm reading this well and that their observations are conclusive, it's M2 macrophages that are involved in the worst cases of COVID19.
Interestingly, the transcription factor NFAT5 which is supposedly increased by dehydration and probably fasting too (also called TonEBP in the literature) tends to suppress the HO-1 enzyme in macrophages.
Moreover, the HO-1 enzyme favor the M2 polarization of macrophages (from the same publication):
"Here, we show that TonEBP suppresses expression of HO-1 by blocking Nrf2 binding to the HO-1 promoter, thereby inducing polarization of macrophages to the M1 phenotype."
Water restriction has been shown to limit the quantity of water from lungs in mice. Would it be sufficient to prevent edema in lungs?