Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells

Benatar, Alejandro Francisco; García, Gabriela Andrea; Búa, Jacqueline; Cerliani, Juan P.; Postan, Miriam; Tasso, Laura Mónica; Scaglione, Jorge; Stupirski, Juan C.; Toscano, Marta A.; Rabinovich, Gabriel A.; Gómez, Karina Andrea

doi:10.1371/journal.pntd.0004148

Cited by 43 publications

(48 citation statements)

References 62 publications

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“…Additionally, interactions between T. vaginalis lipophosphoglycan and Gal1 have been reported to control parasite infection of human cervical epithelial cells (26). Furthermore, low concentrations of Gal1 enhanced T. cruzi replication, whereas higher levels of this lectin inhibited this process (27,28,53). Regarding bacterial infections, Gal4 and Gal8, two-CRD galectins, have been shown to recognize and kill bacteriaexpressing B− blood group antigens on their surface (54).…”

Section: Discussionmentioning

confidence: 99%

“…This includes the N-acetylglucosaminyltransferase 5 (MGAT5), an enzyme that generates β1-6-N-acetylglucosamine (β1-6GlcNAc)-branched complex N-glycans, which are the preferred intermediates for LacNAc extension (19). This prototype lectin has been implicated in glycan-mediated recognition, invasion, and evasion by various pathogens including parasites like Trypanosoma cruzi and Trichomonas vaginalis (25)(26)(27)(28) and viruses such as the human T-cell leukemia virus-1, HIV-1, influenza virus, dengue virus, Epstein-Barr virus, Nipah virus, and Enterovirus 71 (29)(30)(31)(32)(33)(34)(35).…”

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confidence: 99%

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Glycosylation-dependent galectin–receptor interactions promote Chlamydia trachomatis infection

Lujan

Croci

Tudela

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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() constitutes the most prevalent sexually transmitted bacterium worldwide. Chlamydial infections can lead to severe clinical sequelae including pelvic inflammatory disease, ectopic pregnancy, and tubal infertility. As an obligate intracellular pathogen, has evolved multiple strategies to promote adhesion and invasion of host cells, including those involving both bacterial and host glycans. Here, we show that galectin-1 (Gal1), an endogenous lectin widely expressed in female and male genital tracts, promotes infection. Through glycosylation-dependent mechanisms involving recognition of bacterial glycoproteins and -glycosylated host cell receptors, Gal1 enhanced attachment to cervical epithelial cells. Exposure to Gal1, mainly in its dimeric form, facilitated bacterial entry and increased the number of infected cells by favoring - and -host cell interactions. These effects were substantiated in vivo in mice lacking Gal1 or complex β1-6-branched-glycans. Thus, disrupting Gal1--glycan interactions may limit the severity of chlamydial infection by inhibiting bacterial invasion of host cells.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Glycosylation-dependent galectin–receptor interactions promote Chlamydia trachomatis infection

Lujan

Croci

Tudela

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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“…It has been observed that all galectins bind preferentially to the infective stages (amastigotes and trypomastigotes) and that many can promote higher rates of adhesion and infection to host cells and higher rates of infection to mice. In relation to galectin-1, it was observed that the presence of this glycoprotein in human and murine cardiomyocytes is able to prevent infection with trypomastigotes, one more data that goes against the modulating role of galectin in the process of internalization of trypomastigotes [47].…”

Section: T Cruzi Trypomastigote-host Cell Recognitionmentioning

confidence: 99%

How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes

Barrias¹,

Reignault²,

Souza³

2019

Biology OfTrypanosoma Cruzi

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Trypanosoma cruzi, the etiological agent of Chagas disease, is an intracellular parasite that targets specific proteins of the host cell resulting in the generation of a unique parasitophorous vacuole (PV). As an intracellular parasite, T. cruzi interacts with cells from the mammalian host. Here we review aspects related with the binding of the main infective developmental stage (trypomastigote) to the host cell and its recognition by surface-exposed ligands/receptors. This process involves numerous signaling pathways and culminates in the entry of the parasite and modifications in both cells. The invasion of trypomastigotes occurs through multiple endocytic process, assembly of the PV, interaction of this vacuole with the endolysosomal system, lysis of the PV membrane, and multiplication of amastigotes within the cell in direct contact with host cell organelles.assumed that replicating epimastigotes present in the insect gut are not infective to mammalian host. During the vector infection (caused by a hematophagous insect of the family Reduviidae), metacyclic trypomastigotes [8], which penetrate the vertebrate host (several mammals, including man), are released along with their excreta coming in contact with conjunctiva areas or through small lesions in the own site of the bite (favored by the itch caused after the insect's bite). In turn, metacyclic trypomastigotes are able to invade virtually all cell types in the vertebrate host, especially muscle cells, fibroblasts, and macrophages [6]. At this moment, the intracellular cycle of T. cruzi begins, where the firing of several signaling cascades culminates with the closure of the parasitophorous vacuole (PV) where the parasite is found [9,10]. After the PV closure, the process of differentiation of the parasite from the trypomastigote stage to the amastigote stage begins. At the same time, fragmentation of the PV membrane takes place most probably due to the increased concentration of the Tc-Tox perforin-like protein produced by the parasite [11]. After the destruction of the vacuole, the parasite, in the process of differentiation, will be found in the cytoplasm of the host cell where it will initiate its multiplication and subsequent differentiation for trypomastigotes culminating in the rupture of the host cell (Figure 1) [13]. The whole process of formation of the parasitophorous vacuole until its rupture counts on the participation of several organelles of the host cell. Among these, the best characterized is the participation of host cell endosomes and lysosomes. It is the fusion of these organelles with the PV membrane that probably allows the increase or expansion of the PV. In addition, this process is also responsible for the generation of an acidic environment within the PV, which probably will potentiate the action of Tc-Tox and PV membrane fragmentation [13]. Wilkowsky and colleagues [14] have shown that early and late endosomes were critical for vacuole formation. In addition, other organelles responsible for the production of proteins and energy (...

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“…Furthermore, galectin-1 reduces T. cruzi entry into cardiac cells during Chagas disease [261]. Future research studying the mechanism between parasite and galectin-mediated cellular entry is necessary to fully understand how galectins within exosomes may be influencing the innate immune response, particularly in uninfected naïve cells that have not yet been exposed to parasites.…”

Section: Characterization and Quantitative Assessment Of The Exosome mentioning

confidence: 99%

Reciprocal interactions between Leishmania and their microenvironments during infection in the sand fly gut and human macrophages

Kelly¹

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Galectin-1 Prevents Infection and Damage Induced by Trypanosoma cruzi on Cardiac Cells

Cited by 43 publications

References 62 publications

Glycosylation-dependent galectin–receptor interactions promote Chlamydia trachomatis infection

Glycosylation-dependent galectin–receptor interactions promote Chlamydia trachomatis infection

How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes

Reciprocal interactions between Leishmania and their microenvironments during infection in the sand fly gut and human macrophages

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