Plasma membrane repair involvement in parasitic and other pathogen infections

Extracellular Vesicles in Trypanosomatids: Host Cell Communication

“…Gp82 glycoprotein, a metacyclic specific member of the gp85/trans-sialidase family activates mTOR signaling cascades that allow lysosome migration and fusion with the parasitophorous vacuole producing acidification and parasite escape to the cytosol (Cortez et al, 2012;Cortez et al, 2014;Cordero et al, 2019). It also binds to LAMP-2 receptor favoring parasite internalization (Andrade and Andrews, 2005;Albertti et al, 2010;Andrade, 2019). However, previous incubation with EVs released by metacyclic-trypomastigotes decrease invasion of HeLa cells mediated by gp90, another member of the family (Yoshida et al, 1990) and inhibits cell invasion (Rodrigues et al, 2017).…”

Unrevealing the Mystery of Latent Leishmaniasis: What Cells Can Host Leishmania?

“…The Leishmania internalisation could be receptor-mediated (e.g., [ 5 , 30 , 31 , 91 ]), where Leishmania appears to be passively engulfed, or actively initiated by Leishmania promastigote by wounding the host cell plasma membrane [ 8 ], e.g., via the movement of its flagellar tip [ 29 , 43 ]. At least three possible entry pathways have been described ( Figure 1 ): (i) actin-dependent phagocytosis, (ii) caveolin-mediated endocytosis, and (iii) lysosome-triggered endocytosis associated with the host cell plasma–membrane repair mechanism [ 7 , 8 , 28 , 32 , 33 , 34 , 36 , 37 ].…”

“…Passive entry into macrophages appears to be based on the ligand-receptor mediated interactions between the promastigote and macrophage surface molecules [ 5 ]. Contrary to textbook knowledge, Leishmania promastigotes are also able to enter the host cell by an active process using the host cell plasma membrane repair mechanism [ 8 , 28 , 29 ]. The details of the passive and active entry of Leishmania into the professional phagocytes are discussed in the following two subchapters.…”

“…However, Leishmania may also be actively involved in the entry process into the non-canonical host cells, including but not limited to fibroblasts, adipocytes, myofibres or epidermal cells, such as pigmented cells (e.g., [ 8 , 43 , 44 , 45 , 46 ]). Since it is well documented that its close relative T. cruzi uses lysosome exocytosis to invade the host cell, including the non-professional phagocytic cells [ 5 , 38 , 39 ], it is likely that Leishmania could use a similar strategy [ 8 , 28 ].…”

“…While in macrophages, Leishmania -mediated lysosome exocytosis has only been reported after the parasite uptake ( Figure 1 B) [ 29 ]; in different host cells, it can facilitate the invasion process itself ( Figure 1 C) [ 8 , 28 ]. This appears to be the case at least for L. amazonensis entry into the fibroblasts [ 8 ].…”