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Review
. 2021 Oct:23:100456.
doi: 10.1016/j.cophys.2021.06.010. Epub 2021 Jul 6.

Silent hypoxia in COVID-19: a gut microbiota connection

Affiliations
Review

Silent hypoxia in COVID-19: a gut microbiota connection

Akshita B Gopal et al. Curr Opin Physiol. 2021 Oct.

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has triggered the COVID-19 pandemic. Several factors induce hypoxia in COVID-19. Despite being hypoxic, some SARS-CoV-2-infected individuals do not experience any respiratory distress, a phenomenon termed 'silent (or happy) hypoxia'. Prolonged undetected hypoxia could be dangerous, sometimes leading to death. A few studies attempted to unravel what causes silent hypoxia, however, the exact mechanisms are still elusive. Here, we aim to understand how SARS-CoV-2 causes silent hypoxia.

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Figures

Figure 1
Figure 1
Components of the neuronal system involved in O2 sensing. The sagittal view of the brain showing components of the neuronal system involved in sensing O2 level. Vagal afferents and afferent neurons of the glossopharyngeal nerve from the peripheral chemoreceptors reach the medulla and the hypothalamus. Retrotrapezoid nucleus of the medulla contains the central chemoreceptors which is connected to the pre-Bötzinger complex in the medulla oblongata and the cerebellum. Afferent connections from these regions to the thalamus relay the signal to the corticolimbic network that ultimately control ventilatory responses. Areas which are possibly damaged in COVID-19 are colored in magenta. Inset: Decrease in partial pressure of O2 in the blood causes depolarization of the type I glomus cells of the CB and release neurotransmitters.
Figure 2
Figure 2
Summary figure comparing the gut-brain communication during hypoxia in the uninfected and SARS-CoV-2-infected non-dyspneic hypoxic individuals. The gut microbiota is involved in maintaining the intestinal barrier, the BBB integrity as well as overall homeostasis in the host. In COVID-19, SARS-CoV-2-mediated altered inflammatory and metabolic responses damage the intestinal barrier and the BBB. As a result, in the infected individuals, viral particles, increased inflammatory mediators, ROS, neurotropic gut microbial metabolites and depleted SCFA can cause damage to the central and peripheral neurons involved in hypoxia-sensing.

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