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Potentiation of Histamine Release by Microfungal (1→3)‐ and (1→6)‐β‐D‐Glucans
Author(s) -
Holck Peter,
Sletmoen Marit,
Stokke Bjørn Torger,
Permin Henrik,
Norn Svend
Publication year - 2007
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2007.00140.x
Subject(s) - histamine , immunoglobulin e , glucan , long term potentiation , chemistry , laminarin , curdlan , immunology , antibody , biology , biochemistry , pharmacology , polysaccharide , receptor
(1→3)‐β‐D‐Glucans, a cell wall component in most microfungi, are suggested to play a role in the development of respiratory and general symptoms in organic dust‐related diseases. The mechanisms by which they induce these effects are, however, not clear. In the present study, mediator release and its potentiation by the (1→3)‐β‐D‐glucan as well as by the (1→6)‐β‐D‐glucan found in yeast and other fungi were therefore examined. Blood leucocytes from healthy volunteers and from patients allergic to house dust mite were incubated with (1→3)‐β‐D‐glucans with increasing 1,6‐branchings: curdlan [a linear (1→3)‐β‐D‐glucan], laminarin and scleroglucan, and furthermore with pustulan, a linear (1→6)‐β‐D‐glucan. Histamine release was not observed on exposure to the glucans only, but in the presence of anti‐immunoglobulin E (IgE) antibody or specific antigens, all the glucans investigated led to an enhancement of the IgE‐mediated histamine release. The glucans induced a significant potentiation of the mediator release when present at concentrations in the range of 2–5 × 10 −5 M. These results suggest that (1→3)‐β‐D‐glucan as well as (1→6)‐β‐D‐glucan aggravates IgE‐mediated histamine release. Knowledge concerning the effects of glucans on immune responses may be of importance for understanding and treating inflammatory and allergic diseases.