Boysenberry ingestion supports fibrolytic macrophages with the capacity to ameliorate chronic lung remodeling

• Published in: American journal of physiology. Lung cellular and molecular physiology Vol. 311; no. 3; pp. L628 - L638
• Main Authors: Shaw, Odette M, Hurst, Roger D, Harper, Jacquie L
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.09.2016
• Subjects: Airway Remodeling; Animals; Asthma - diet therapy; Asthma - immunology; Asthma - physiopathology; Berries; Collagen - metabolism; Diet; Fruit; Leukocytes; Lung - immunology; Lung - pathology; Lungs; Macrophages, Alveolar - immunology; Male; Matrix; Matrix Metalloproteinase 9 - metabolism; Mice, Inbred C57BL; Rodents; Rubus; chronic lung fibrosis; fibrolytic macrophages; airway remodeling; fruit consumption
• ISSN: 1040-0605; 1522-1504
• DOI: 10.1152/ajplung.00309.2015

Lung fibrosis negatively impacts on lung function in chronic asthma and is linked to the development of profibrotic macrophage phenotypes. Epidemiological studies have found that lung function benefits from increased consumption of fruit high in polyphenols. We investigated the effect of boysenberry consumption, in both therapeutic and prophylactic treatment strategies in a mouse model of chronic antigen-induced airway inflammation. Boysenberry consumption reduced collagen deposition and ameliorated tissue remodeling alongside an increase in the presence of CD68+CD206+arginase+ alternatively activated macrophages in the lung tissue. The decrease in tissue remodeling was associated with increased expression of profibrolytic matrix metalloproteinase-9 protein in total lung tissue. We identified alternatively activated macrophages in the mice that consumed boysenberry as a source of the matrix metalloproteinase-9. Oral boysenberry treatment may moderate chronic tissue remodeling by supporting the development of profibrolytic alternatively activated macrophages expressing matrix metalloproteinase-9. Regular boysenberry consumption therefore has the potential to moderate chronic lung remodeling and fibrosis in asthma and other chronic pulmonary diseases.