Abstract
β-Glucan is a polysaccharide that can be extracted from fungal cell walls. Wellmune WGP®, a preparation of β-1,3/1,6-glucans, is a dietary supplement that has immunomodulating properties. Here we investigated the effect WGP had on a mouse model of asthma. OVA-induced asthma in mice is characterized by infiltration of eosinophils into the lung, production of Th2 cytokines and IgE. Daily oral administration of WGP (400 µg) significantly reduced the influx of eosinophils into the lungs of OVA-challenged mice compared to control mice. In addition, WGP inhibited pulmonary production of Th2 cytokines (IL-4, IL-5, IL-13), however serum IgE levels were unaffected by WGP treatment. These data indicate that WGP could potentially be useful as an oral supplement for some asthma patients, however, it would need to be combined with therapies that target other aspects of the disease such as IgE levels. As such, further studies that examine the potential of WGP in combination with other therapies should be explored.Electronic supplementary materialThe online version of this article (doi:10.1186/s40064-016-2501-1) contains supplementary material, which is available to authorized users.
Highlights
Asthma is a chronic inflammatory airway disease that is caused by an allergic response in many cases
Β-Glucan, a fungal cell wall extract, is marketed as a dietary supplement that can promote immune balance (Wichers 2009). β-Glucans are found in the cell walls of fungi, plants and some bacteria. β(1-3)- or β(1-6)-linked glucans are recognized by the Dectin-1 receptor
We demonstrated that daily oral administration of WGP reduces eosinophil influx into the lungs and the production of Th2 cytokines (IL-4, IL-5, IL-13) compared to control mice
Summary
Asthma is a chronic inflammatory airway disease that is caused by an allergic response in many cases. It affects 5–10 % of the population and is associated with significant morbidity and mortality (Barnes 2008). It is characterized by airway inflammation, airway hyperresponsiveness (AHR) and mucus production (Holgate 2012). Lung inflammation is caused by infiltration of eosinophils and T cells secreting Th2-cytokines (IL-4, IL-5, IL-13) into the lung. Dectin 1 is a type II transmembrane C-type lectin-like receptor, which recognizes both soluble and particulate β-glucans (Brown 2006; Brown et al 2002, 2003). While Dectin-1 can bind both soluble and particulate β-glucans, only particulate β-glucans activate Dectin-1 signaling and responses (Goodridge et al 2011). β-Glucan-induced signaling through Dectin-1 promotes Th1 and Th17 responses (Leibundgut-Landmann et al 2008)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
