The lectin ArtinM activates RBL-2H3 mast cells without inducing degranulation

• Published in: PloS one 2020-03, Vol.15 (3), p.e0230633-e0230633
• Main Authors: Buranello, Patricia A A, Barbosa-Lorenzi, Valéria C, Pinto, Marcelo R, Pereira-da-Silva, Gabriela, Barreira, Maria Cristina R A, Jamur, Maria Célia, Oliver, Constance
• Format: Article
• Language: English
• Subjects: Acceleration; Allergic reactions; Allergy; Artocarpus heterophyllus; Biology and Life Sciences; Cell activation; Cell cycle; Cell proliferation; Connective tissues; Cytokines; Degranulation; EDTA; Histamine; Homeostasis; Hypersensitivity; Immune response; Immunomodulation; Immunotherapy; Inflammation; Interleukin 6; Jackfruit; Laboratories; Lectins; Life sciences; Low concentrations; Mast cells; Medical schools; Medicine and Health Sciences; Microscopy; Molecular biology; NF-AT protein; NF-κB protein; Pathogens; Phenols (Class of compounds); Phosphorylation; Physical characteristics; Physical Sciences; Physiological aspects; Scientific equipment industry; Therapeutic applications; Tyrosine; Wound care; Wound healing
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0230633

Mast cells are connective tissue resident cells with morphological and functional characteristics that contribute to their role in allergic and inflammatory processes, host defense and maintenance of tissue homeostasis. Mast cell activation results in the release of pro-inflammatory mediators which are largely responsible for the physiological functions of mast cells. The lectin ArtinM, extracted from Artocarpus heterophyllus (jackfruit), binds to D-manose, thus inducing degranulation of mast cells. ArtinM has several immunomodulatory properties including acceleration of wound healing, and induction of cytokine release. The aim of the present study was to investigate the role of ArtinM in the activation and proliferation of mast cells. The rat mast cell line RBL-2H3 was used throughout this study. At a low concentration (0.25μg/mL), ArtinM induced mast cell activation and the release of IL-6 without stimulating the release of pre-formed or newly formed mediators. Additionally, when the cells were activated by ArtinM protein tyrosine phosphorylation was stimulated. The low concentration of ArtinM also activated the transcription factor NFkB, but not NFAT. ArtinM also affected the cell cycle and stimulated cell proliferation. Therefore, ArtinM may have therapeutic applications by modulating immune responses due to its ability to activate mast cells and promote the release of newly synthesized mediators. Additionally, ArtinM could have beneficial effects at low concentrations without degranulating mast cells and inducing allergic reactions.