Differential effect of plant lectins on mast cells of different origins

Abstract

Histamine release induced by plant lectins was studied with emphasis on the carbohydrate specificity, external calcium requirement, metal binding sites, and mast cell heterogeneity and on the importance of antibodies bound to the mast cell membrane to the lectin effect. Peritoneal mast cells were obtained by direct lavage of the rat peritoneal cavity and guinea pig intestine and hamster cheek pouch mast cells were obtained by dispersion with collagenase type IA. Histamine release was induced with concanavalin A (Con A), lectins from Canavalia brasiliensis, mannosespecific Cymbosema roseum, Maackia amurensis, Parkia platycephala, Triticum vulgaris (WGA), and demetallized Con A and C. brasiliensis, using 1-300 µg/ml lectin concentrations applied to Wistar rat peritoneal mast cells, peaking on 26.9, 21.0, 29.1, 24.9, 17.2, 10.7, 19.9, and 41.5%, respectively. This effect was inhibited in the absence of extracellular calcium. The lectins were also active on hamster cheek pouch mast cells (except demetallized Con A) and on Rowett nude rat (animal free of immunoglobulins) peritoneal mast cells (except for mannose-specific C. roseum, P. platycephala and WGA). No effect was observed in guinea pig intestine mast cells. Glucose-saturated Con A and C. brasiliensis also released histamine from Wistar rat peritoneal mast cells. These results suggest that histamine release induced by lectins is influenced by the heterogeneity of mast cells and depends on extracellular calcium. The results also suggest that this histamine release might occur by alternative mechanisms, because the usual mechanism of lectins is related to their binding properties to metals from which depend the binding to sugars, which would be their sites to bind to immunoglobulins. In the present study, we show that the histamine release by lectins was also induced by demetallized lectins and by sugar-saturated lectins (which would avoid their binding to other sugars). Additionally, the lectins also released histamine from Rowett nude mast cells that are free of immunoglobulins. Correspondence

Immunostimulatory activity of ConBr: a focus on splenocyte proliferation and proliferative cytokine secretion

“…Protein carbohydrate interactions occur in a number of biochemical processes in a variety of different cell types including lymphocytes, mast cells, macrophages and neutrophils Lopes et al 2005;Alencar et al 2007;Figueiredo et al 2009). These interactions are believed to serve as major signals in these cells, stimulating the release of proinflammatory mediators such as leukotrienes, NO and cytokines (Benjamin et al 1997), including IL-1, IL-6, IL-10, TNF-α and GMCSF ).…”

“…ConBr has previously been shown to induce the following effects: proliferation and IFN-γ production in cultured peripheral blood mononuclear cells (Barral-Netto et al 1992); nitric oxide (NO) production by murine macrophages in vitro and in vivo (Andrade et al 1999); in vivo lymphocyte activation and apoptosis ); IFN-γ, IL-10, IL-4, granulocyte macrophage colony-stimulating factor (GMCSF) and TNF-α production in human peripheral blood mononuclear cells ; and histamine release from mast cells (Lopes et al 2005).…”

ConBr, a Lectin from Canavalia brasiliensis Seeds, Protects Against Quinolinic Acid-Induced Seizures in Mice

“…[31]. Moreover, ConBr showed different biological effects than ConA with respect to peripheral biological activities [11], including induction of rat paw edema [51], peritoneal macrophage spreading in the mouse [52], in vivo human lymphocyte stimulation [53], induction of histamine release [54,55] and NO release [56]. Thus, it is possible that differences in the quaternary conformation of ConBr, as compared with ConA, may be the basis for these divergent phenotypes [30].…”

Cordia verbenacea and secretion of mast cells in different animal species

“…The concanavalin A, in turn induces the release of histamine interacting with residual sugar and metals on the surface of mast cells, however, the release is not primarily to the immune system, meaning that the presence of immunoglobulin E in conjunction with mast cells is not essential for the secretory stimulus occurs (Lopes et al, 2005).…”