A Comparison of the Pulmonary Inflammatory Potential of Different Components of Yeast Cell Wall*

Abstract

1-->3-Beta-glucan has been associated with pulmonary inflammation induced by exposure to fungal or yeast cell wall dust. 1-->3-Beta-glucan is the major cell wall component of yeast or fungi. However, the yeast cell wall contains several other components besides 1-->3-beta-glucans, such as mannan and chitin. Few studies evaluated the contribution of these other cell wall components to pulmonary inflammation. The present study compares a crude particulate yeast cell wall preparation (zymosan A) to purified yeast glucan, purified yeast glucan mannan, or purified yeast glucan chitin particles for their potency to induce mouse pulmonary inflammation after in vivo exposure. Mannan is the second most abundant polysaccharide in the yeast cell wall, whereas chitin content is a minor component. The results show that pulmonary injury is mediated by both chitin and 1-->3-beta-glucan and to a lesser degree by mannan. There is also evidence that zymosan is more potent than purified 1-->3-beta-glucan alone. Evidence indicates that 1-->3-beta-glucan is the major inflammatory component in yeast and fungal cell walls.

Adjuvant effect of zymosan after pulmonary treatment in a mouse ovalbumin allergy model

“…It has been reported that zymosan has distinct biological activities compared to purified yeast particulate 1→3-β-glucan [13]. A recent study by Huang et al [28] indicated that the adjuvant activity of purified 1→3-β-glucan led to a Th1/Th17 response, and not the Th2 response as reported in this paper and by others [14][15][16] for zymosan, further differentiating the activities of 1→3-β-glucan from zymosan.…”

“…Zymosan has been shown to induce lung inflammation [9], alter adaptive immune response [10], and affect lung clearance of a bacterial pathogen [11,12] after pulmonary treatment when evaluated using an animal model. In a comparison of the pulmonary inflammatory potential of different components of yeast and fungal cell walls, 1→3-β-glucan was the most potent inflammatory agent tested, and zymosan, the crude B-glucan preparation, had a greater inflammatory activity than a partially purified particulate 1→3-β-glucan [13]. In addition, specific β-glucans [14,15] and soluble mold extracts [16] have been observed to have adjuvant effects in an allergic response to ovalbumin (OVA) in mice.…”

The relationship between Candida species cultured from the respiratory tract and systemic inflammation in critically ill patients with ventilator-associated pneumonia

“…[26][27][28] Studies with Pneumocystis jiroveci and fungi have demonstrated that ß-glucans can stimulate the release of inflammatory markers, such as IL-1 and TNF-a, through NF-jB activation, trigger fungicidal responses, and generate reactive oxygen intermediates. [29][30][31][32] These observations provide a mechanism by which Candida may play a causal role in the increased inflammatory markers and may potentiate worse clinical outcomes.…”

Antibody-Mediated Protection through Cross-Reactivity Introduces a Fungal Heresy into Immunological Dogma

“…Attempts to harness immunomodulators as antimicrobial agents underscore the fact that infectious diseases are a manifestation of host damage stemming from hostmicrobe interactions and that many infectious diseases result in similar immunopathology and damage. For example, fungal beta-glucans are highly inflammatory (45). Therefore, although antibodies to beta-glucans inhibit fungal growth in vitro, their effect in vivo may be as immunomodulators, because their activity prevents the development of inflammation.…”