ArticleThe American journal of pathology2014
Preferential lymphatic growth in bronchus-associated lymphoid tissue in sustained lung inflammation.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Spatially Resolved Heterogeneity of Lymphatic Vasculature in the Adult Lung-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Lung Lymphatics in Edema, Inflammation, and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- The thrombin receptor PAR1 orchestrates changes in lymphatic endothelial cell junction morphology to augment lymphatic drainage during lung injury.Nature cardiovascular research · 2025Article
- Tertiary Lymphoid Structures in Tuberculosis: Persistence, Protection, and Pathology.Immunological reviews · 2025Review
- Three-dimensional visualization of an unusual pulmonary lymphoproliferation after COVID-19.SAGE open medical case reports · 2025Article
- Loss of Lymphatic IKKα Disrupts Lung Immune Homeostasis, Drives BALT Formation, and Protects against Influenza.ImmunoHorizons · 2024Article
- Mycoplasma pneumoniae pneumonia-associated thromboembolism with plastic bronchitis: a series of five case reports and literature review.Italian journal of pediatrics · 2024Review
- Establishment of a Mouse Model ofMicroorganisms · 2024Article
- Single Cell Analysis of Lung Lymphatic Endothelial Cells and Lymphatic Responses during Influenza Infection.Journal of respiratory biology and translational medicine · 2024Article
- Review
- The lymphatic vasculature in lung function and respiratory disease.Frontiers in medicine · 2023Review
- Lung lymphatic thrombosis and dysfunction caused by cigarette smoke exposure precedes emphysema in mice.Scientific reports · 2022Article
- T cell activation niches-Optimizing T cell effector function in inflamed and infected tissues.Immunological reviews · 2022Review
- Pro-lymphangiogenic VEGFR-3 signaling modulates memory T cell responses in allergic airway inflammation.Mucosal immunology · 2021Article
- Lymphatic drainage from bronchus-associated lymphoid tissue in tolerant lung allografts promotes peripheral tolerance.The Journal of clinical investigation · 2020Article
- Lymphatic Proliferation Ameliorates Pulmonary Fibrosis after Lung Injury.The American journal of pathology · 2020Article
- Role of iBALT in Respiratory Immunity.Current topics in microbiology and immunology · 2020Review
- Engineering drug delivery systems to overcome mucosal barriers for immunotherapy and vaccination.Tissue barriers · 2020Article
- Inducible Bronchus-Associated Lymphoid Tissue (iBALT) Attenuates Pulmonary Pathology in a Mouse Model of Allergic Airway Disease.Frontiers in immunology · 2020Article
- Adventitial Cuffs: Regional Hubs for Tissue Immunity.Trends in immunology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Lymphatics proliferate, become enlarged, or regress in multiple inflammatory lung diseases in humans. Lymphatic growth and remodeling is known to occur in the mouse trachea in sustained inflammation, but whether intrapulmonary lymphatics exhibit similar plasticity is unknown. We examined the time course, distribution, and dependence on vascular endothelial growth factor receptor (VEGFR)-2/VEGFR-3 signaling of lung lymphatics in sustained inflammation. Lymphatics in mouse lungs were examined under baseline conditions and 3 to 28 days after Mycoplasma pulmonis infection, using prospero heomeobox 1-enhanced green fluorescence protein and VEGFR-3 as markers. Sprouting lymphangiogenesis was evident at 7 days. Lymphatic growth was restricted to regions of bronchus-associated lymphoid tissue (BALT), where VEGF-C-producing cells were scattered in T-cell zones. Expansion of lung lymphatics after infection was reduced 68% by blocking VEGFR-2, 83% by blocking VEGFR-3, and 99% by blocking both receptors. Inhibition of VEGFR-2/VEGFR-3 did not prevent the formation of BALT. Treatment of established infection with oxytetracycline caused BALT, but not the lymphatics, to regress. We conclude that robust lymphangiogenesis occurs in mouse lungs after M. pulmonis infection through a mechanism involving signaling of both VEGFR-2 and VEGFR-3. Expansion of the lymphatic network is restricted to regions of BALT, but lymphatics do not regress when BALT regresses after antibiotic treatment. The lung lymphatic network can thus expand in sustained inflammation, but the expansion is not as reversible as the accompanying inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.