Abstract
A previous study revealed that fucoidan inhibited mast cell degranulation through the upregulation of galectin-9 in blood. The purpose of this study is to elucidate its mechanism using ovalbumin (OVA) induced anaphylaxis model mice (BALB/c, Female, 5-week-old) and mast cell line (RBL-2H3 cells). Oral administration of fucoidan after sensitization with OVA/Al(OH)3 inhibited reduction of rectal temperature induced by activation of mast cells. Fucoidan increased galectin-9 mRNA expression only in colonic epithelial cells. These results suggested that fucoidan could suppress the allergic symptoms in sensitized mice by inducing galectin-9 production from colonic epithelial cells. In addition, to check the influence of galectin 9 on the degranulation of mast cells, RBL-2H3 cell lines were treated directly with recombinant galectin-9. As expected, galectin-9 inhibited degranulation of RBL-2H3 cells pre-bound with IgE. Moreover, the residual amounts of IgE on RBL-2H3 cells were decreased by an addition of galectin-9. It was demonstrated that galectin-9 could remove IgE even if IgE was already bound to mast cells and suppress the mast cells degranulation induced by antigen. This study shows that fucoidan might become an effective therapeutic agent for patients already developed type I allergic diseases.
Highlights
Allergy is the abnormal immune reaction against specific substances contained in foods, pollens, animal dander, latex, house-dust-mite fecal particle and so on [1]
It was shown that the intravenous administration of anti-galectin-9 antibody canceled the suppressive effect of fucoidan in the passive cutaneous anaphylaxis (PCA) model. These results suggest that fucoidan might suppress activation of mast cells through promoting production of galectin-9 from intracellular epithelial cells (IECs)
Though Lgals9 levels were increased only in colon by oral administration of fucoidan after 2nd and 4th sensitization, no drastic differences recognized in the other tissues. These results suggested that IECs, especially colonic epithelial cells might be responsible for production galectin-9 responded to fucoidan
Summary
Allergy is the abnormal immune reaction against specific substances (allergens) contained in foods, pollens, animal dander, latex, house-dust-mite fecal particle and so on [1]. Type I allergy, which is characterized with immediate hypersensitivity reactions, is mediated by interaction between immunoglobulin E (IgE) and antigen resulting in release of mediators including histamine. The degraded antigens are presented by major histocompatibility complex class II (MHC II) to T cell receptors (TCRs) on naïve CD4+ T cells [4,6]. The complex induces activation of mast cells and a number of inflammatory mediators, including histamine, lipid-derived mediators, cytokines and chemokines are released from mast cells [7]. These mediators induce allergic reaction, such as tissue swelling, erythema and sneezing [1]. Type I allergic diseases, including food allergy, allergic rhinitis and asthma, are major health problems around the world and patients suffering from these diseases are ever increasing, so that effective therapy for type I allergy is required to cure them
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