Oxytocin’s anti-inflammatory and proimmune functions in COVID-19.

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Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19) respiratory disease, has triggered a worldwide pandemic infecting over 16 million people, killing over 600,000, and causing extensive economic and social disruption. COVID-19 is an infectious disease that is rapidly spreading and is associated with a significant mortality rate. While most cases show mild respiratory symptoms (fever, cough, shortness of breath, and fatigue), some progress to viral pneumonia, cardiovascular complications, and multiorgan failure, often associated with a “cytokine storm”.

Cytokine storm is an escalating inflammatory response associated with COVID-19 disease severity and mortality. Cytokine storms are characterized by a severe inflammatory response triggering a series of immune responses that causes changes in lymphocytes, which can rapidly progress into acute respiratory distress syndrome (ARDS), damage to the alveolar lumen, often followed by multiorgan failure. Damage to T lymphocytes along with the cytokine storm are important factors that lead to exacerbations of patients’ cases. Severe cases are associated with decreased levels of total CD4+/CD8+ T lymphocytes compared with mild cases, while clinical improvement is associated with an increase in CD8+ T cells. Patients in the intensive care unit (ICU) display higher plasma concentrations of cytokines and chemokines [interleukin-6 (IL-6), IL-2, IL7, IL10 and TNF-α] compared with non-ICU patients. Today, there are no Food and Drug Administration (FDA)-approved drugs that are specifically targeting COVID-19 disease. Remdesivir and corticosteroids are showing promising results for severe cases, while no drugs have been suggested for hospitalized patients in early moderate phases. Repurposing existing drugs that can act on the adaptive immune response and prevent the cytokine storm in early phases of the disease is a priority.

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