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Nathan W

School of Education & Human Sciences Annika Semoe, Erie, Pennsylvania

In the lungs, after entering in type II alveolar cells, SARS-CoV-2 infected cells become defective for surfactant production (Ghati et al., 2021) and release cytokines, like IL-8 among others, which in turn activate alveolar macrophages to release IL-1, IL-6, and TNF-, that induce natural killer and dendritic cell differentiation and macrophage M1 polarization, enhancing the proinflammatory response with increased vasodilation causing neutrophil and activated T cell influx from the capillaries into the alveolus, all leading to the cytokine storm (Carcaterra and Caruso, 2021

J Paediatr Child Health

Similarly, inhibition of CD38 in aged mice boosted NAD + levels, improving exercise capacity, but in this case, no significant changes in mitochondrial biogenesis-related genes were observed 138

Atherosclerosis as pathogenetic substrate for Sars-Cov 2 cytokine storm