Abstract
In this review, we discuss spatiotemporal kinetics and inflammatory signatures of innate immune cells specifically found in response to SARS-CoV-2 compared to influenza virus infection. Importantly, we cover the current understanding on the mechanisms by which SARS-CoV-2 may fail to engage a coordinated type I response and instead may lead to exaggerated inflammation and death. This knowledge is central for the understanding of available data on specialized pro-resolving lipid mediators in severe SARS-CoV-2 infection pointing toward inhibited E-series resolvin synthesis in severe cases. By investigating a publicly available RNA-seq database of bronchoalveolar lavage cells from patients affected by COVID-19, we moreover offer insights into the regulation of key enzymes involved in lipid mediator synthesis, critically complementing the current knowledge about the mediator lipidome in severely affected patients. This review finally discusses different potential approaches to sustain the synthesis of 3-PUFA-derived pro-resolving lipid mediators, including resolvins and lipoxins, which may critically aid in the prevention of acute lung injury and death from COVID-19.
Highlights
GENERAL CONCEPTS OF SARS-CoV-2 INFECTION AND ASSOCIATED INFLAMMATIONCOVID-19, the infectious disease caused by the novel coronavirus SARS-CoV-2, currently represents a worldwide medical, economic, social, and political challenge (Mahase, 2020)
INNATE IMMUNITY IN INFLUENZA VIRUS INFECTION. Despite both bearing the potential of causing a severe infection of the lung, influenza and SARS-CoV-2 elicit several pathways of innate immunity that differ in many aspects
We found a decrease in ALOX5AP expression levels in macrophages and DCs in bronchoalveolar lavage fluid (BALF) from severe COVID-19 patients, whereas RNA expression of this central activating protein tended to be increased in neutrophils of patients affected by severe disease (Figure 3)
Summary
COVID-19, the infectious disease caused by the novel coronavirus SARS-CoV-2, currently represents a worldwide medical, economic, social, and political challenge (Mahase, 2020). SARS-CoV-2 patients suffering from a complicated course of infection either fail to exert a robust, interferon (IFN)-mediated anti-viral response in the early phase of infection and present with an overwhelming immune activation termed as “cytokine storm” (Blanco-Melo et al, 2020; Fu et al, 2020). The latter is defined by increased levels of circulating cytokines accompanied by systemic and pulmonary immune cell activation in a similar setting as described in subjects suffering from ARDS or sepsis (Wilson et al, 2020). This review will initially focus on innate immunity in influenza and in SARS-CoV-2 infection comparing the respective host immune signatures, and subsequently depict recent findings on the mediator lipidome in COVID-19
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