Lysosomes are acidic organelles that are not only involved in degradation processes but also participated in other cellular functions, such as specialized secretion and plasma membrane (PM) resealing. When the PM is ruptured, Ca2+ flows from the extracellular milieu toward the cytoplasm potentially triggering cell death. In order to escape from the apoptotic route, cells developed an elegant mechanism in which lysosomes are recruited to the sites of injuries in a Ca2+-dependent fashion. Lysosomes, fuse with the PM releasing their enzymatic content. Acid sphingomyelinase (ASM), one of the secreted enzymes, cleaves sphingomyelin into ceramide, inducing compensatory endocytosis and internalization of the membrane-damaged site. Trypanosoma cruzi, the etiological agent of Chagas disease, relies heavily on lysosomes to successfully invade mammalian cells. By mechanically injuring the host PM, T. cruzi evokes lysosome exocytosis, and subsequently, compensatory endocytosis. The latter drives the parasite into the host cell, where it can replicate. This early association with lysosomes prevents T. cruzi evasion from the host cells allowing colonization of host intracellular milieu. This review chapter will summarize the main contributions in the field exploring the crosstalk between PM repair and T. cruzi invasion and how the understanding of these mechanisms evolved throughout the years.
Part of the book: Lysosomes