Renin Angiotensin System, Gut-Lung Cross Talk and Microbiota. Lessons from SARS-CoV Infections

Abstract

The two antagonistic systems of angiotensin converting enzyme (ACE)-1 and ACE-2 are in the “eye of the hurricane” of severe acute respiratory syndrome coronavirus (SARS-CoV-2). The receptor of the SARS-CoV-2 is the same as ACE-2, which causes its under-expression after binding it, followed by the internalization of the complex virus-ACE-2. ACE-2 have multiple functions with specially relevance in cardiovascular diseases. Furthermore, the non-enzymatic role of ACE-2 gives rise to a Hartnup disease, a phenocopy involving microbiota. With this chapter, we intent to explore the key pathways involved in SARS-CoV-2 infection, from the host perspective, considering our hypothesis related to transporter of neutral amino acids, which includes tryptophan precursor of serotonin and kynurenine.

Gut microbiota and renin-angiotensin system: a complex interplay at local and systemic levels

“…Ample evidence indicates that SARS-CoV-2 infection causes a defect of the gut-blood barrier, increasing the penetration of microbes, bacterial lipopolysaccharide, or peptidoglycan into the circulation, possibly disrupting the immunological reaction to COVID-19 infection, and resulting in multisystem dysfunction or septic shock ( 139 , 142 , 143 ). It was suggested that in the pathogenesis of SARS-CoV-2, any disturbances in host-microbiota crosstalk could act as an initiating or reinforcing factor ( 144 ).…”