Cross-Linking Mast Cell Specific Gangliosides Stimulates the Release of Newly Formed Lipid Mediators and Newly Synthesized Cytokines

Filho, Edismauro Garcia Freitas; Silva, Elaine Zayas Marcelino da; Zanotto, Camila Ziliotto; Oliver, Constance; Jamur, Maria Célia

doi:10.1155/2016/9160540

Cited by 10 publications

(9 citation statements)

References 50 publications

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“…Also, stimulation through receptors other than FcεRI can result in selective mediator release. For example, activation of Toll-like receptors (TLR) [17,54] or ganglioside cross-linking [55,56] on the mast cell surface leads to cytokine production and release in the absence of degranulation. Furthermore, chemokines do not induce mast cell degranulation, but they are able to induce the secretion of newly-synthesized mediators [57].…”

Section: Plos Onementioning

confidence: 99%

“…The binding of many of these ligands such as SCF (stem cell factor), CCL3 (CC-chemokine ligand 3) and PAMPs (pathogenassociated molecular patterns) results in selective mediator release without degranulation [63]. Furthermore, cross-linking GD1b derived gangliosides on the surface of RBL-2H3 cells causes the release of newly formed and newly synthesized mediators without degranulation [55].…”

Section: Plos Onementioning

confidence: 99%

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

et al. 2020

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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.

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Section: Plos Onementioning

confidence: 99%

Section: Plos Onementioning

confidence: 99%

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

et al. 2020

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“…Also, rodent MCs express α-galactosyl derivatives of the ganglioside GD1b (90). Antibodies recognizing this ganglioside inhibit degranulation and histamine release by modulating FcεRI endocytosis (90, 91) but in contrast, are also able to promote release of cytokines and lipid mediators (92).…”

Section: Membrane Lipid Organizing Enzymes Are Targets To Modulate Mamentioning

confidence: 99%

Modulation of Mast Cell Reactivity by Lipids: The Neglected Side of Allergic Diseases

et al. 2019

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Mast cells (MCs) have long been mainly regarded as effector cells in IgE-associated allergic disorders with potential immunoregulatory roles. Located close to the allergen entry sites in the skin and mucosa, MCs can capture foreign substances such as allergens, toxins, or noxious substances and are exposed to the danger signals produced by epithelial cells. MC reactivity shaped by tissue-specific factors is crucial for allergic responses ranging from local skin reactions to anaphylactic shock. Development of Th2 response leading to allergen-specific IgE production is a prerequisite for MC sensitization and induction of FcεRI-mediated MC degranulation. Up to now, IgE production has been mainly associated with proteins, whereas lipids present in plant pollen grains, mite fecal particles, insect venoms, or food have been largely overlooked regarding their immunostimulatory and immunomodulatory properties. Recent studies, however, have now demonstrated that lipids affect the sensitization process by modulating innate immune responses of epithelial cells, dendritic cells, and NK-T cells and thus crucially contribute to the outcome of sensitization. Whether and how lipids affect also MC effector functions in allergic reactions has not yet been fully clarified. Here, we discuss how lipids can affect MC responses in the context of allergic inflammation. Direct effects of immunomodulatory lipids on MC degranulation, changes in local lipid composition induced by allergens themselves and changes in lipid transport affecting MC reactivity are possible mechanisms by which the function of MC might be modulated.

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“…It has also been shown that elevated expression levels of GM3, GM2, GM1 and GD1a can be observed during maturation of the human mast cell line HMC-1 [44] and that exogenous GM3 inhibits interleukin (IL)-3-stimulated cell proliferation of bone marrow-derived mouse mast cells [45]. In addition, it has been reported that cross-linking of GD1b-derived gangliosides activates RBL-2H3, a rat mast cell line, leading to the release of inflammatory cytokines, such as IL-4, IL-6 and TNFα [46].…”

Section: Inflammatory Cells and Gangliosidesmentioning

confidence: 99%

Vascular Diseases and Gangliosides

Sasaki

Toyoda

2019

IJMS

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Vascular diseases, such as myocardial infarction and cerebral infarction, are most commonly caused by atherosclerosis, one of the leading causes of death worldwide. Risk factors for atherosclerosis include lifestyle and aging. It has been reported that lifespan could be extended in mice by targeting senescent cells, which led to the suppression of aging-related diseases, such as vascular diseases. However, the molecular mechanisms underlying the contribution of aging to vascular diseases are still not well understood. Several types of cells, such as vascular (endothelial cell), vascular-associated (smooth muscle cell and fibroblast) and inflammatory cells, are involved in plaque formation, plaque rupture and thrombus formation, which result in atherosclerosis. Gangliosides, a group of glycosphingolipids, are expressed on the surface of vascular, vascular-associated and inflammatory cells, where they play functional roles. Clarifying the role of gangliosides in atherosclerosis and their relationship with aging is fundamental to develop novel prevention and treatment methods for vascular diseases based on targeting gangliosides. In this review, we highlight the involvement and possible contribution of gangliosides to vascular diseases and further discuss their relationship with aging.

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Cross-Linking Mast Cell Specific Gangliosides Stimulates the Release of Newly Formed Lipid Mediators and Newly Synthesized Cytokines

Cited by 10 publications

References 50 publications

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

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

Modulation of Mast Cell Reactivity by Lipids: The Neglected Side of Allergic Diseases

Vascular Diseases and Gangliosides

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