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Mechanisms involved in ArtinM-induced suppression of human neutrophil apoptosis

Ricci-Azevedo, Rafael; Roque-Bareira, Maria Cristina; Girard, Denis . Mechanisms involved in ArtinM-induced suppression of human neutrophil apoptosis In: 12ème colloque du centre de recherche Biomed, 5 mai 2016, Centre de congrès Palace, Laval (Québec).

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Résumé

The most effective measures to prevent infectious diseases are clean water, good hygiene practices, and vaccination. Nonetheless, vaccines are not currently available for all human pathogens. Although the traditional antigens - based vaccines have not shown success against intracellular pathogens, the called anti - infective therapies have shown some promising results against this. Basically, these approaches aim to target toll - like receptors (TLRs), and thereby, they prepare the immune system to fight appropriately against these types of pathogens. ArtinM is a lectin from Artocarpus heterophyllus , which is endowed of immunomodulatory capacity. Under experimental conditions, ArtinM already has been shown to induce protection against Leishmania major , Paracoccidioides braziliensis , Candida albicans , among others. Because ArtinM binds to TLR2 and other unknown glycoproteins on the surface of immune cells, thus activating them, we believe that ArtinM represents a future anti - infective tool. Concerning neutrophils, ArtinM is known to induce their migration, L - selectin shedding and interleukin (IL) - 8, IL - 1 β, LTB4 and TNF - α secre- tion; which ultimately potentiates the phagocytic and microbicide capacity of these cells. Recently, it has been shown that ArtinM delays human neutrophil apoptosis. Although ArtinM increases survival of non - infected neutrophils, the mechanism by which the lectin acts is still unclear. Because the neutrophil survival rate is crucial both to infectious diseases and inflammatory conditions, and that ArtinM can induce protection against intracellular pathogens, it is mandatory to understand the mechanisms involved in ArtinM - induced suppression of neutrophil apoptosis. Therefore, we performed western blot experiments to determine if the cell signaling events involving AKT, ERK - 1/2 and p38 are important for ArtinM - induced suppression of neutrophil apoptosis. The results indicate that ArtinM treatment, differently from the cytokine GM - CSF, does not activate ERK - 1/2 at the time points investigated (1 - 90 minutes of stimulation). On the other hand, ArtinM, as well as GM - CSF, was able to activate AKT and p38. Furthermore, we were interested in answering whether or not ArtinM could alter de novo protein synthesis in human neutrophils. Interestingly, after 24h of incubation with ArtinM, neutrophils were found to synthesis neo - polypeptides when compared to untreated cells. Experiments using the potent protein synthesis inhibitor, cycloheximide, are currently in progress in our laboratory in order to determine the role of de novo protein synthesis in Artin - M - induced suppression of neutrophil. The results obtained during this project allow us to conclude presently that AKT and p38, but not ERK - 1/2, are part of the cell signaling events activated by ArtinM in neutrophils and that this lectin is a potent inducer of de novo protein synthesis.

Type de document: Document issu d'une conférence ou d'un atelier
Informations complémentaires: Présentation par affiche
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Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 25 déc. 2017 23:15
Dernière modification: 25 déc. 2017 23:15
URI: http://espace.inrs.ca/id/eprint/6623

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