Arabinogalactan isolated from cowshed dust extract protects mice from allergic airway inflammation and sensitization

Mice were treated during sensitization and airway challenge with 50 μg CDE, high-molecular-mass fraction (P1), 1 μg arabinogalactan (AG) isolated from P1, or supernatant of the Yariv precipitation. Subsequently, mice were evaluated for eosinophilic airway inflammation (A), cytokine production (B), and IgE levels (C). Results are presented as means with SDs (n = 4). ∗P < .05.

Mice were treated during sensitization and airway challenge with either extract from A pratensis or arabinogalactan (AG) isolated from this extract. Subsequently, mice were evaluated for eosinophilic airway inflammation (A), cytokine production (B), and IgE production in BAL fluid (C). Results are presented as means with SDs (n = 4). ^∗P < .05.

Mice were either sham-treated (n = 10) or treated by intranasal application of 5 μg arabinogalactan (AG; n = 10). Airway hyperreactivity was measured invasively. Means ± SEMs are shown ^∗P < .05; ^∗∗P < .01; ^∗∗∗P < .001 (A). Subsequently, lung sections were stained by Alcian blue/periodic acid-Schiff reagent (B). Goblet cells were counted in 4 different lung slices from each mouse and given as cells per millimeter basement membrane. Means ± SDs are shown (n = 5).

Mice were treated by inhalation of arabinogalactan (AG) isolated from gum arabic or larch during sensitization and airway challenge with OVA. Subsequently, mice were evaluated for eosinophilic airway inflammation (A), IL-5 production (B), and IgE production in BAL fluid (C). Results are presented as means with SDs (n = 4).

Analysis of activity of arabinogalactan (AG) from A pratensis on mouse BMDCs. A, IL-10 production of BMDCs in vitro after stimulation with 10 μg/mL AG. B and C, AG-treated or untreated BMDCs were used to sensitize mice via the airways. After challenge of mice, they were evaluated for eosinophilic airway inflammation (B) and cytokine production of splenic lymphocytes (C). Median is shown.

One dimensional hydrogen-1 NMR spectrum of AG from A pratensis (27°C, deuterated water) (A) and of arabinogalactan (AG) from Larix (B). The anomeric protons of α- L-Araf, β-L-Araf, and β-D-Galp residues are labeled.

Analysis of activity of arabinogalactan (AG) treated with oxalic acid at 60°C, 18 hours, or control treated by omitting oxalic acid. Mice were treated by inhalation of AG during sensitization and airway challenge. Subsequently, mice were evaluated for eosinophilic airway inflammation (A), IL-5 production (B), and OVA-specific IgE in BAL fluid (C). Means with SDs are shown (n = 5). ^∗P < .05; ^∗∗P < .01.

Depiction of treatment protocol. OVA i.p., Systemic immunization with OVA adsorbed in aluminum hydroxide. OVA-aerosol, Challenges with 1% OVA aerosol via the airways. AR, Measurements of airway responsiveness. Analysis, Harvest of BAL cells, serum, and splenocytes for analysis. i.n., Intranasal.

LPS was applied to mice intranasally during sensitization and airway challenge with ovalbumin. Subsequently mice were evaluated for eosinophilic airway inflammation (A), IL-5 production (B), and IgE production in BAL fluid (C). Results are presented as means with SDs calculated from 4 mice per group.

Neutralization of produced IL-10 partially restores sensitizing capacity of arabinogalactan (AG)–treated BMDCs. BMDCs were treated with AG, and released IL-10 was blocked by a IL-10–neutralizing antibody (OVA + AG + anti–IL-10). Control cells were treated with AG in the presence of an isotype control antibody. Subsequently, cells were used to sensitize mice via the airways. Three days after challenge with OVA aerosol, all mice were evaluated for eosinophilic airway inflammation.