Abstract
Inflammatory disorders are associated with the activation of tryptophan (TRYP) catabolism via the kynurenine pathway (KP). Several reports have demonstrated the role of KP in the immunopathophysiology of both leprosy and coronavirus disease 19 (COVID-19). The nervous system can be affected in infections caused by both Mycobacterium leprae and SARS-CoV-2, but the mechanisms involved in the peripheral neural damage induced by these infectious agents are not fully understood. In recent years KP has received greater attention due the importance of kynurenine metabolites in infectious diseases, immune dysfunction and nervous system disorders. In this review, we discuss how modulation of the KP may aid in controlling the damage to peripheral nerves and the effects of KP activation on neural damage during leprosy or COVID-19 individually and we speculate its role during co-infection.
Highlights
During severe COVID-19, there is an increase in the inflammatory status caused by a cytokine storm (Hu et al, 2021; Yang et al, 2021)
The increase in pro-inflammatory mediators in COVID-19 and in leprosy may increase the activity of the enzyme Indoleamine 2,3dioxygenase 1 (IDO1), which results in the production of kynurenine metabolites (Belladonna and Orabona, 2020; Turski et al, 2020)
M. leprae induces the expression of a variety of genes related to innate immunity in Schwann cells strains in the early stage of infection, even before there were gene modifications associated with reprogramming in progenitor/stem-like cells (pSLCs)
Summary
During severe COVID-19, there is an increase in the inflammatory status caused by a cytokine storm (Hu et al, 2021; Yang et al, 2021). M. leprae induces the expression of a variety of genes related to innate immunity in Schwann cells strains in the early stage of infection, even before there were gene modifications associated with reprogramming in pSLC.
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