A rampage through the body

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Science  24 Apr 2020:
Vol. 368, Issue 6489, pp. 356-360
DOI: 10.1126/science.368.6489.356

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  • Relevance of barrier protection in COVID-19, especially in the lung
    • Wolfgang Liedtke, Professor of Neurology, Anesthesiology and Neurobiology, Duke University Health System, Durham NC, US
    • Other Contributors:
      • Sven-Eric Jordt, Associate Professor of Anesthesiology and Pharmacology, Duke University Health System, Durham NC, USA
      • Wolfgang Kuebler, Professor of Physiology and Respiratory Medicine, Charite Universitaetsmedizin, Berlin, Germany

    The article is highly interesting and timely, yet it barely mentions one cardinal feature and key pathogenic event in COVID-19, i.e. lung barrier failure and the subsequent emergence of lung edema.
    The above reporting portrays a minority of critically-ill COVID-19 patients with low blood oxygen levels and discrepant lack of shortness of breath as pointing to an excessive constriction of the lung´s blood vessels. That is one interpretation. Another interpretation is permeability type lung edema caused by viral pneumonia which has damaged the alveolo-capillary barrier of the lung’s microcirculation. As a result, fluid leaks from blood vessels into the lung to a degree that oxygen exchange is already impaired whereas the exchange of carbon dioxide – the main driver of shortness of breath - is still intact. The new Lancet pathologic-anatomic findings of SARS-CoV-2-mediated inflammatory injury to endothelial cells in autopsied COVID-19 patients support this concept (Endothelial Cell Infection and Endotheliitis in COVID-19, The Lancet, April 17, 2020; https://doi.org/10.1016/S0140
    We thus believe that protecting the integrity of the alveolo-capillary barrier and other capillary barriers should be made one key principle of treating COVID-19, in addition to antivirals and immuno-modulators. Barrier protection may contain COVID-19, a primarily respiratory infection, from systemically affecting vital org...

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    Competing Interests: None declared.
  • RE: Neuronal strategies to mitigate COVID19 - associated cytokine storm?

    This Feature article gives an impressive update of the “rampage through the body” of COVID19 infection, mediated by a systemic hyper-inflammation and cytokine storm in multiple organs, including the nervous system (1).
    In addition to being a possible target of infection, the nervous system may also be involved to activate anti-inflammatory strategies to mitigate complications of viral infection. In fact, the vagus nerve can regulate the immune responses to infections, inhibiting cytokine release and ameliorating inflammation-mediated injury in a variety of cytokine-dependent models of inflammatory disease (2). This inhibitory neural circuit, i.e. the cholinergic anti-inflammatory pathway, utilizes acetylcholine that interacts with the α7 subunit of the nicotinic acetylcholine receptor expressed on cytokine-producing macrophages in the spleen (3).
    As reminded by Wadman et al. (1), a possible way of access to the nervous system for COVID19 is through the nose and the olfactory bulb. With such a way of diffusion, the first brain target could be the orbitofrontal cortex, i.e. a region involved in the regulation of activation of the parasympathetic system (4). Damage to this region could, therefore, contribute to the “sympathetic storm”, with hypo-activation of the parasympathetic and hyper-activation of the sympathetic system, described in some COVID19-affected patients.
    We hypothesize that activation of the parasympathetic vagal circuits may open therapeutic...

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    Competing Interests: None declared.

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