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Fig. 1 | Immunity & Ageing

Fig. 1

From: UGRP1-modulated MARCO+ alveolar macrophages contribute to age-related lung fibrosis

Fig. 1

Airway epithelial cells upregulated UGRP1 expression responsible for the high level of CCL6 in the aged lungs. The lung tissues of aged mice (20–24 months old) were compared with those of young mice (10–16 weeks old). A Expression levels of UGRP1 in airway epithelial cells detected by immunohistochemistry. The arrows indicate the UGRP1 positive cells in the lung tissues. Scale bar, 100 μm (upper) or 25 μm (blow). B UGRP1+ cell numbers in the lung tissues. Each symbol represents the average of 10 fields of vision (20 ×) from an individual sample. C The expression levels of UGRP1 in the bronchoalveolar lavage fluid (BALF, 1.0 mL/mouse) were detected by ELISA. There were 6 mice in each group. D Expression levels of UGRP1 and CCL6 in the lung tissues detected by western blotting. Data were normalized relative to the expression level of β-actin protein in the same sample. There were 3 mice in each group. E Young mice were treated with UGRP1 (15 μg/mouse, once a week for two weeks), and then the expression levels of CCL6 in the serum, lung tissues and BALF (1.0 mL/mouse) were detected by ELISA. There were 6 mice in each group. Data are shown as the mean ± SEM. Comparisons by unpaired two-tailed Student’s t-test. *p < 0.05, **p < 0.01, **** p < 0.0001

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