Leprosy is a chronic infectious disease caused by Mycobacterium leprae or
Mycobacterium lepromatosis. Dermal tissue macrophages and Schwann cells from
peripheral nerves are the main host cells for the pathogen. The clinical manifestations
of this disease depend basically on the host’s immune response to M. leprae. However,
genes relevant to both innate and adaptive immune responses also seem to contribute to
leprosy acquisition and to determine its clinical forms. The crucial clinical problem in
leprosy is represented by episodes of intense inflammation. They represent a major
problem in the course of leprosy, as reactional episodes can be responsible for
permanent damage to nerves, causing deformities. Among bacterial pathogens,
infection of peripheral nerves is a unique property of M. leprae. The intensity of the
inflammatory reaction in response to tissue damage caused by pathogens is strongly
associated with mitochondria and their respective mitochondrial DNA, since this
organelle and its constituents act as potent ligands for several innate immunity
receptors. In this chapter, we will first describe the general context of leprosy and its
various clinical forms, diagnosis and treatment, highlighting episodes of acute
inflammatory response during this pathology and, finally, we will outline some cellular
mechanisms that lead to neurodegenerative consequences in leprosy. The literature
partially attributes these to cytokines and, mainly, to TNF-α, as well as to changes in
mitochondrial dynamics, especially mitochondrial DNA, when mitochondrial
dysfunction seems to be involved in the pathogenesis of neuritis in leprosy.
Keywords: Leprosy, Mitochondrial dysfunction, Neuritis.
