Coronavirus-induced diseases have afflicted humanity for several decades. This scenario was aggravated by the emergence of the coronavirus disease 2019 (named COVID-19) in Wuhan, China, in December 2019. Since then, COVID-19 has killed millions of people worldwide, probably the most devastating pandemic since HIV/AIDS. This review aimed to bring together important updated aspects related to coronavirus-induced diseases and the enhanced vascular permeability observed mainly in the lungs of affected people. The dysregulated vascular permeability in the lungs is of fundamental importance for coronaviruses-caused morbidity and mortality. Thus, as described in this review, it is a target of new and old drugs.

Sepsis is a grave systemic condition that affects several organs and is caused by an infectious disease. Among the organs targeted by sepsis is the brain, a condition named sepsis-associated encephalopathy (SAE). Epidemiological studies indicate that 25%–70% of sepsis patients develop SAE, presenting acute and chronic symptoms. The main acute symptom is delirium, while chronic symptoms include cognitive impairment, locomotor dysfunction and mood disorders, amongst them, depression. The physiopathology of SAE involves systemic and local actions. Systemically, reduced brain perfusion, hyperglycemia, and activation of the sensory vagus nerve contribute to SAE. Locally, inflammation, enhanced oxidative stress, and enhanced excitotoxicity play vital roles in SAE development. Today, there is no commercially available treatment for SAE. We recently demonstrated that twenty-nanometer citrate-capped gold nanoparticles (cit-AuNP) intravenously injected two or four hours after induction of sepsis could reduce cerebral inflammation in mice. In the present study, we showed that cit-AuNP acutely injected in mice with sepsis exhibited faster clinical symptom resolution and reduced glutamate levels in the brain thirty days after sepsis induction. The acute twenty-nanometer cit-AuNP treatment also prevented depression-like behavior in mice after a sepsis episode. Thus, cit-AuNP therapy may potentially be used to prevent sepsis-induced depression.