“…Similarly, C. albicans hyphal extension facilitates phagosomal rupture and allows transient access to the cytoplasm and a rise in pH. Here, constant lysosomal fusions are required to repair the phagolysosomal lesions quickly [154] , [155] , [156] , [157] . Fig.…”
Section: Host Adaptation and Immune Evasion Mechanismsmentioning
“…Similarly, C. albicans hyphal extension facilitates phagosomal rupture and allows transient access to the cytoplasm and a rise in pH. Here, constant lysosomal fusions are required to repair the phagolysosomal lesions quickly [154] , [155] , [156] , [157] . Fig.…”
Section: Host Adaptation and Immune Evasion Mechanismsmentioning
“…The putative protective role of LNCA and lysosomal fusion in this pathway (3b) is based on the known ability of lysosomes to “patch up”, (i.e., prevent rupture of) cellular membranes, (e.g., [ 118 , 119 ]). Specifically, this hypothetical mechanism was suggested by analogy with the role of lysosomes in preventing/repairing rupture of phagosomes (see [ 119 ] and associated commentary [ 120 ]). Such a stabilising action of lysosomes could allow an endocytic vacuole to retain its content until autolysis of trypsin and destruction of other digestive enzymes is completed.…”
Section: Endocytic Vacuoles: Actination Rupture and Lap-like Non-cano...mentioning
Recent studies have highlighted the importance of autophagy and particularly non-canonical autophagy in the development and progression of acute pancreatitis (a frequent disease with considerable morbidity and significant mortality). An important early event in the development of acute pancreatitis is the intrapancreatic activation of trypsinogen, (i.e., formation of trypsin) leading to the autodigestion of the organ. Another prominent phenomenon associated with the initiation of this disease is vacuolisation and specifically the formation of giant endocytic vacuoles in pancreatic acinar cells. These organelles develop in acinar cells exposed to several inducers of acute pancreatitis (including taurolithocholic acid and high concentrations of secretagogues cholecystokinin and acetylcholine). Notably, early trypsinogen activation occurs in the endocytic vacuoles. These trypsinogen-activating organelles undergo activation, long-distance trafficking, and non-canonical autophagy. In this review, we will discuss the role of autophagy in acute pancreatitis and particularly focus on the recently discovered LAP-like non-canonical autophagy (LNCA) of endocytic vacuoles.
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