Place of Circulating Biomarkers and Respiratory Eicosanoids in the Prognosis of Severe Forms of Covid-19 Pneumonia

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The reason for the involvement of overweight in the severity of viral respiratory pathologies, particularly during influenza and coronavirus infections, has been the subject of numerous studies which have made it possible to objectify the importance of viral load (at least in mice), particularly in ...

The reason for the involvement of overweight in the severity of viral respiratory pathologies, particularly during influenza and coronavirus infections, has been the subject of numerous studies which have made it possible to objectify the importance of viral load (at least in mice), particularly in the lower airways and in the alveolar sacs, leading to tissue alteration and alveolar haemorrhage. The mechanisms responsible for alveolar damage during viral pathologies, particularly Coronavirus, are very similar to those observed during acute respiratory distress syndromes in adults. In many situations, endotoxin (or lipopolysaccharide, LPS) plays a major role in the pathophysiology and even the severity of respiratory damage, in particular due to the existence of circulating endotoxin from the causative pathogen (Gram-negative bacteria), but also due to translocation of digestive origin in the context of sepsis (systemic inflammatory response) which is associated with (if not responsible for) respiratory aggression. The importance of this mechanism during pulmonary aggression of viral origin is however unknown. This respiratory attack is associated with a major systemic inflammatory response, reported during the course of Covid-19 infection as corresponding to a "cytokine storm". However, the course of the inflammation is poorly understood and its prognostic nature in the occurrence of a secondarily severe form is not yet better illustrated. The inflammatory reaction (cytokines, eicosanoids, etc.) is an essential process for the elimination of pathogens by the host, but it must be limited in intensity and duration, otherwise it becomes deleterious for the infected organ. In the case of the lungs, it can induce an acute respiratory distress syndrome (ARDS), which can be severe as in Covid-19 patients with complications. It can be hypothesized that in the early stages of infection, these mediators may play a protective role against Covid-19. Inhibition of these mediators may therefore be deleterious as has been observed in subjects who have taken non-steroidal anti-inflammatory drugs (NSAIDs) that inhibit the production of eicosanoids.

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