(Biomedical and Biophysical Research Communication (2006) 350:501-507)

Type I hypersensitivity, similar to food allergy, is once invaded allergen (causative agent of allergy) into the body. IgE is generated from B cell that is one of the immune cells. IgE binds to the mast cell, and then the allergen binds to the IgE antibody. Since allergen binds to IgE antibodies, it releases chemical substances such as histamine from mast cells. And as a result, it causes allergic symptoms such as skin inflammation, eczema, and sneezing. Therefore, it is essential to control IgE antibodies for suppressing allergy symptoms. This study will closely examine how Fucoidan stops food allergy to activate the required part of the immune response.

First of all, I want to explain the mechanism of  IgE binds to mast cells by using Masashi Mizuno et al., research.  The degraded antigen is presented by a primary histocompatibility complex class II (MHC II) to the T cell receptor (TCR) on naive CD4 + T cells. Hence, CD4 + T cells are activated and develop into type 2 T helper (Th2) cells. Th2 cells secrete Th2 cytokines such as interleukin (IL) -4 and IL-13 and are involved in the IgM-to-IgE class switching of immunoglobulins in B cells. Antigen-specific IgE produced by B cells sensitizes mast cells by binding to the IgE high-affinity receptor (FcεRI) expressed on the surface of mast cells. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072523/

The development of type I allergy is connected to some immune cells, especially mast cells.

According to “Fucoidan suppress CE germline transcription and NFkB inversion for IgE production in B cells Fucoidan and Food allergy” by Souich Oomisuet al., Fucoidan, a dietary fiber contained in seaweed, suppresses the increase in antigen-specific IgE in mice exposed to ovalbumin.

This study investigated the effect of Fucoidan on B cell IgE production and intracellular events in vitro. IgE antibodies are synthesized IL-4 and anti-CD40 antibodies (the antibody binds to CD40 protein on the B cells surface) to stimulate B cells. Researchers examined the number of IgE expressions to add Fucoidan to produce the B cells at a high concentration of the anti- CD40 antibody and IL-4.

As a result, this observation suggests that IgE expression with Fucoidan is lower than one without Fucoidan. (Fig. 1a) However, when B cells are stimulated by a low concentration of anti-CD40 antibody and a high concentration of IL-4, Fucoidan did not show inhibited the production of IgE. (Fig. 1, b)

Hence as the experiment concludes, the researchers demonstrate that the possibility of fucoidan suppressing either one of the signaling pathways that depend on CD40 or IL-4. Fucoidan inhibited the signal pathway that relies on CD40 than the signal pathway depending on IL-4.