Yeast β-glucan soluble effect really better than insoluble ? not likely!

Orally administered β-glucans induced phagocytic activity, oxidative bursts, and IL-1 production of peritoneal macrophages in mice [26]. A higher phagocytic activity

and oxidative metabolism of neutrophils and monocytes, indicating an immune restoring activity of yeast β-glucan has also been shown in rats [27]. However, not only the

cellular but also the humoral acute phase immune reaction is affected by yeast β-glucan feeding as shown by increased lysozyme and ceruloplasmin activitiy [28].

Moreover, oral delivery of β-glucans impact mucosal immunity, as shown by an increase of intraepithelial lymphocytes in the intestine of mice [29]. In rats, the 

absorption of soluble β-glucans translocated from the gastrointestinal tract into the systemic circulation leads to an increased immune response and resistance against

infectious challenge [16]. The effect of an insoluble β-glucan against anthrax infection in mice showed that the treated animals survived the anthrax infection, while

50% of the control animals died, indicating an improved immune function in animals fed with β-glucan [30].

Another important aspect to be considered is the solubility of β-glucans, as soluble and particulate (insoluble) β-glucans isolated from yeast may stimulate the immune system via different pathways [31]. In vivo and in vitro studies revealed that particulate (insoluble) β-glucan was phagocytosed by dendritic cells and macrophages via dectin-1 receptor pathway.

 Although particulate β-glucans can also be taken up by dendritic cells through a dectin-1 receptor independent mechanism, the dectin-1 receptor

pathway is essential for the activation of dendritic cells, which in turn induces T-cell response and cytokine release [31]. However, not all insoluble particulate β-glucans are

able to bind to and activate the dectin-1 receptor. Studies with synthetically produced β-glucans revealed that binding to dectin-1 receptor is specific for β-glucans with a

(1,3)-beta backbone. Backbones with mixed (1,3)/(1,4)-β-bindings (e.g. barley derived β-glucans) are not recognized by this receptor. Also, a backbone length of at least seven

glucose units is required for binding, in addition to one (1,6)-β-side-chain branch (e.g. insoluble yeast β-glucans). Furthermore, the binding activity increases with increasing molecular weight of the polymer [32]. However, binding to the dectin-1 receptor alone does not activate the signal cascade induced by this receptor. Indeed, dectin-1 signaling and the concomitant immune responses are only activated by particulate β-glucans but not by soluble β-glucans [33]. Insoluble, particulate β-glucans 

induced the process of phagocytosis, resulting in the elimination of invading microbes by binding to the dectin-1 receptor [31]. Further, particulate β-glucans

promotes T-cell differentiation into Th1-cells and enhances cytotoxic T lymphocyte priming by the dectin-1 pathway. Even though soluble β-glucans are also recognized by the

dectin-1 receptors, they cannot activate immune response via this pathway. Soluble β-glucans are, however, able to bind to the CR3 receptor. The activation of the CR3 leads

to complement system mediated immune process, supported by specific antibodies [31].

These results show that different β-glucan particles influence the immune system via different pathways. Insoluble β-glucans are able to activate both the innate and the adaptive immune responses, whereas soluble β-glucans are most effective via the complement system, which needs specific antibodies.

26. Suzuki I, Tanaka H, Kinoshita A, Oikawa S, Osawa M, Yadomae T: Effect of orally administered beta-glucan on macrophage function in mice.

 Int J Immunopharmacol 1990, 12:675–684.

27. Wojcik R: Effect of Biolex Beta-HP on phagocytic activity and oxidative metabolism of peripheral blood granulocytes and monocytes in rats intoxicated by cyclophosphamide. 

Pol J Vet Sci 2010, 13:181–188.

28. Małaczewska J, Wójcik R, Jung L, Siwicki AK: Effect of Biolex β-HP on selected parameters of specific and non-specific humoral and cellular

immunity in rats. Bull Vet Inst Pulawy 2010, 54:75–80.

29. Tsukada C, Yokoyama H, Miyaji C, Ishimoto Y, Kawamura H, Abo T:Immunopotentiation of intraepithelial lymphocytes in the intestine by

oral administrations of beta-glucan. Cell Immunol 2003, 221:1–5.

30. Vetvicka V, Terayama K, Mandeville R, Brousseau P, Kournikakis B, Ostroff G:Orally-administered yeast β1,3-glucan Prophylactically protects against

anthrax infection and cancer in mice. J Am Nutraceutical Ass 2002,5(2):16–20.

31. Qi C, Cai Y, Gunn L, Ding C, Li B, Kloecker G, Qian K, Vasilakos J, Saijo S,Iwakura Y, Yannelli JR, Yan J: Differential pathways regulating innate and

adaptive antitumor immune responses by particulate and solubleyeast-derived beta-glucans. Blood 2011, 117:6825–6836.