An animal model for allergic penicilliosis induced by the intranasal instillation of viable Penicillium chrysogenum conidia

Abstract

Background-A study was undertaken to determine the consequences of long term intranasal instillation of Penicillium chrysogenum propagules in a mouse model. Methods-C57 Black/6 mice were inoculated intranasally each week for six weeks with 10 4 viable and non-viable P chrysogenum conidia. Cytokine levels and cellular responses in these animals were then measured. 4 non-viable conidia group and the controls. When proteins were extracted from P chrysogenum conidia, attached to microtitre plates and incubated with serum from the 10 4 viable group, significant increases in conidia-specific IgE and IgG 1 were observed compared with controls, while serum from the 10 4 non-viable group was similar to controls. Conclusions-These data suggest that long term inhalation of viable P chrysogenum propagules induces type 2 T helper cell mediated (Th2) inflammatory responses such as increases in total and conidia-specific serum IgE and IgG 1 , together with BAL fluid levels of IL-4 and IL-5 and peripheral and airway eosinophilia, which are mediators of allergic reactions. (Thorax 2000;55:489-496) Results-Compared

Detection of AirborneStachybotrys chartarumMacrocyclic Trichothecene Mycotoxins on Particulates Smaller than Conidia

“…Numerous research groups have tried to determine the underlying cause(s) of SBS and poor IAQ. Fungi and their secondary metabolites, such as mycotoxins, are hypothesized contributors that have been closely examined (3,5,6,9,18,21). The fungi isolated from buildings with poor IAQ include a wide variety of genera and species.…”

Increased Neurotrophin Production in aPenicillium chrysogenum-Induced Allergic Asthma Model in Mice

“…However, the number of viable conidia used in other animal studies is compared to the doses used in this study in terms of induction of allergic responses. Schwab et al (2003) and Cooley et al (2000) reported that exposure to low levels (10 2 viable conidia) of P. chrysogenum did not induce significant lung inflammation or increased serum immunoglobulins (Schwab et al, 2003) while exposure to 10 4 P. chrysogenum conidia induced type 2 T-helper-cell-mediated inflammatory responses as well as allergic responses (Cooley et al, 2000). These studies support a threshold level for induction of allergic responses.…”

“…The Penicillium species of mold, especially P. chrysogenum, are common indoor contaminants and are associated with asthma (Chou et al, 2003). Several investigators demonstrated that exposure of animals to viable conidia of P. chrysogenum induced allergic asthma responses, including increased serum immunoglobulin (Ig) E and airway eosinophilia (Cooley et al, 2000;Schwab et al, 2003). Recently, our group demonstrated that multiple exposures to P. chrysogenum extract (PCE) induced dose-dependent responses characteristic of allergic asthma such as airway eosinophilia, increased specific IgE, and airway hyperresponsiveness (Chung et al, 2005).…”

The sick building syndrome as a part of the autoimmune (auto-inflammatory) syndrome induced by adjuvants

“…Some of the minor criteria suggested by Shoenfeld for ASIA are also met in SBS patients: ''the appearance of antibodies directed at the suspected adjuvant, or in some cases auto-antibodies'' [36][37][38][39]; patients with documented exposure to molds in SBS have elevated titers of antibodies (IgA, IgM, and IgG) to neural-specific antigens when compared with healthy controls [36]. In a mouse model, exposure to molds caused a significant increase in total serum IgG(2a) and interferon gamma [37], and the presence of serum IgE specific to fungi was found to be connected with building-related syndrome in individuals working in damp and moldy buildings [39].…”