Investigation of the heterogeneity and cellular plasticity in chronic injury induced by Thalassophryne nattereri venom

Abstract

Venomous fish are responsible for numerous accidents involving humans in the north and northeast regions of Brazil, Thalassophryne nattereri being the most common of them. T. nattereri venom causes chronic inflammation, impaired tissue repair and muscle necrosis in poisoned victims. In the inflammatory process, some cells such as neutrophils, monocytes and macrophages are recruited by inflammatory mediators for control and repair of the injury, but studies developed previously by our group show that the venom of T. nattereri develops an inappropriate cellular inflammatory response characterized by a reduced number of neutrophils at the site of injury. Infiltration of neutrophils and their subsequent elimination by macrophages after apoptosis is the prerequisite for the resolution of inflammatory processes, and knowing that the T. nattereri venom and its main toxin Natterins alter the normal process of leukocyte recruitment into the tissue allowing the persistence the lesion becomes necessary to extend our studies of the cellular events responsible for the transition from acute inflammatory response without resolution for a persistent, chronic and pathological settings. To gain new insights into the mechanisms of venom pathogenesis and to further elucidate the role of its major toxins, Natterins this work aims to investigate the profile of cellular response mainly of phagocytic and antigen-presenting cells (macrophages and dendritic cells) and Treg cells on the inflamed tissue and in draining lymphoid organs, to determinate the kinetic, number and the activation state. (AU)