Mitochondrial Dysfunction in Leprosy: Shedding Light on the Neurodegenerative Consequences

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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.