Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation
J. Clin. Invest. Peter Baluk, et al. 115:247 doi:10.1172/JCI22037 [Go to this article.]

Figure 4
VEGF-C and VEGF-D in M. pulmonis–infected airways. Immunohistochemical staining of VEGF-C (A–C) and VEGF-D (D–F) in mouse airways and lung 14 days after infection. (A) VEGF-C (green) in epithelium, peribronchial inflammatory cells, and type II alveolar epithelial cells (asterisks) of lung. Blood vessels stained for CD31 (red). (B) VEGF-C (green) in inflammatory cells (arrows) near sprouting lymphatic vessels (red) in tracheal whole mount. (C) Colocalization of VEGF-C immunoreactivity (green) and F4/80 immunoreactivity (red) in macrophages (yellow, arrows). (D) Strong VEGF-D staining (green) of neutrophils in airway lumen. (E) VEGF-D–positive neutrophils (boxed area in D) shown at higher magnification in airway lumen (arrows, green) and airway smooth muscle cells (arrowheads). Blood vessels stained for CD31 (red). (F) VEGF-D immunoreactivity in neutrophils (arrows, green) in tracheal mucosa near sprouting lymphatic vessels (arrowheads) stained for VEGFR-3 (red). Scale bar in F applies to all figures: 200 μm in A and D and 50 μm in B, C, E, and F. (G) Results of RT-PCR analysis showing higher expression of mouse mRNA for VEGF-C (mVEGF-C) and VEGF-D in tracheas after 14 days of infection.