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This collaborative group investigated the factors triggering lymphangiogenesis in response to increased leakage in airway inflammation. They used mouse models with chronic respiratory tract infections with Mycoplasma pulmonis and models with adenoviral transduction of airway epithelium with VEGF family growth factors.
In pathogen free mice, blood and lymphatic vessels form discrete segmented networks. In mice infected with M pulmonis, lymphangiogenesis started to occur at 7 days and, by the end of 2 weeks, lymphatic vessels were more abundant than blood vessels. As VEGFR-3 is thought to mediate lymphangiogenesis, the mice were treated with VEGFR-3-Ig or a functional anti-VEGFR-3 antibody. Lymphatic growth was almost completely prevented in the first week of infection (96% reduction and 87% reduction in lymphatic sprouts, respectively). Treatment with antibodies against VEGFR-1 or VEGFR-2 had no effect on growth of lymphatic vessels after M pulmonis infection. Inoculation with VEGF adenovirus did not promote lymphangiogenesis but inoculation with VEGF-C and VEGF-D adenovirus did.
Lymphatic sprouting stopped during treatment with antibiotics and steroids; however, the network of new lymphatic vessels did not decrease, even after 12 weeks. Failure of lymphangiogenesis after infection impaired fluid drainage and immune cell transport to local lymph nodes and promoted bronchial lymphoedema. VEGFR-3, VEGF-C and VEGF-D are important in lymphangiogenesis accompanying some types of bronchial inflammation. Further studies are needed to look at factors that stimulate and inhibit lymphatic growth, as restoration of lymphangiogenesis may complement conventional treatments for inflammatory airway disease.
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