Uvnäs-Moberg, Kerstin
- Department of Applied Animal Science and Welfare, Swedish University of Agricultural Sciences
Research article2020Peer reviewedOpen access
Imami, Ali S.; O'Donovan, Sinead M.; Creeden, Justin F.; Wu, Xiaojun; Eby, Hunter; McCullumsmith, Cheryl B.; Uvnas-Moberg, Kerstin; McCullumsmith, Robert E.; Andari, Elissar
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a worldwide pandemic, infecting over 16 million people worldwide with a significant mortality rate. However, there is no current Food and Drug Administration-approved drug that treats coronavirus disease 2019 (COVID-19). Damage to T lymphocytes along with the cytokine storm are important factors that lead to exacerbation of clinical cases. Here, we are proposing intravenous oxytocin (OXT) as a candidate for adjunctive therapy for COVID-19. OXT has antiinflammatory and proimmune adaptive functions. Using the Library of Integrated Network-Based Cellular Signatures (LINCS), we used the transcriptomic signature for carbetocin, an OXT agonist, and compared it to gene knockdown signatures of inflammatory (such as interleukin IL-1 beta and IL-6) and proimmune markers (including T cell and macrophage cell markers like CD40 and ARG1). We found that carbetocin's transcriptomic signature has a pattern of concordance with inflammation and immune marker knockdown signatures that are consistent with reduction of inflammation and promotion and sustaining of immune response. This suggests that carbetocin may have potent effects in modulating inflammation, attenuating T cell inhibition, and enhancing T cell activation. Our results also suggest that carbetocin is more effective at inducing immune cell responses than either lopinavir or hydroxychloroquine, both of which have been explored for the treatment of COVID-19.
COVID19; oxytocin; immune; LINCS; transcriptomic signature
Physiological Genomics
2020, Volume: 52, number: 9, pages: 401-407 Publisher: AMER PHYSIOLOGICAL SOC
Immunology in the medical area
DOI: https://doi.org/10.1152/physiolgenomics.00095.2020
https://res.slu.se/id/publ/108293