Full Title: Boysenberry and apple juice concentrate reduces acute lung 1 inflammation through increased alternatively activated macrophage activity in 2 an acute mouse model of allergic airways disease Bioactive compounds such as anthocyanins, proanthocyanins and other polyphenols

: are found in a wide variety of fruits and vegetables, and consumption of these have 18 been associated with reduced lung inflammation and improved lung function in 19 asthma and other lung diseases. We investigated whether a combination of 20 Boysenberry and apple juice, found in BerriQi® Boysenberry and apple juice 21 concentrate, could reduce the allergic airways inflammation associated with asthma. 22 We characterised the polyphenolic components in BerriQi® Boysenberry and apple 23 juice concentrate and identified the main compounds as cyanidin glycosides, 24 ellagitannins, and chlorogenic acid. We found that consumption of 2.5 mg/kg of total 25 anthocyanins from the BerriQi® Boysenberry and apple juice concentrate 26 significantly reduced eosinophil infiltration following acute ovalbumin (OVA) exposure 27 in a mouse model of allergic airways inflammation. We found that BerriQi® 28 Boysenberry and apple juice concentrate consumption increased M2 (CD206+) 29 macrophages and the production of the M2-associated cytokines CXCL10 and CCL4 30 within the lung. These results suggest that consumption of BerriQi® Boysenberry 31 and apple juice concentrate promotes a shift towards an anti-inflammatory 32 environment within the lung leading to reduced immune cell infiltration and tissue 33 damage. 34 airways inflammation. Our results show that consumption of mg/kg TAC BerriQi® Boysenberry and apple juice concentrate reduced We found that mice that BerriQi® cell in and this could be as a result of a shift towards an anti-inflammatory environment within the lung. These results highlight the potential of anthocyanin-rich Boysenberry and apple dietary supplementation to modulate innate immune pathways during acute allergic lung inflammation. Further work is needed to determine if these pathways are also altered in other lung inflammatory conditions, such as air pollution exposure. Clinical studies are needed to show if these findings are translatable to human