Your browser doesn't support javascript.
loading
Preferential lymphatic growth in bronchus-associated lymphoid tissue in sustained lung inflammation.
Baluk, Peter; Adams, Alicia; Phillips, Keeley; Feng, Jennifer; Hong, Young-Kwon; Brown, Mary B; McDonald, Donald M.
Afiliación
  • Baluk P; Department of Anatomy, the Cardiovascular Research Institute, and the Comprehensive Cancer Center, University of California, San Francisco, California. Electronic address: peter.baluk@ucsf.edu.
  • Adams A; Department of Anatomy, the Cardiovascular Research Institute, and the Comprehensive Cancer Center, University of California, San Francisco, California.
  • Phillips K; Department of Anatomy, the Cardiovascular Research Institute, and the Comprehensive Cancer Center, University of California, San Francisco, California.
  • Feng J; Department of Anatomy, the Cardiovascular Research Institute, and the Comprehensive Cancer Center, University of California, San Francisco, California.
  • Hong YK; Departments of Surgery, Biochemistry, and Molecular Biology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California.
  • Brown MB; Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, Florida.
  • McDonald DM; Department of Anatomy, the Cardiovascular Research Institute, and the Comprehensive Cancer Center, University of California, San Francisco, California.
Am J Pathol ; 184(5): 1577-92, 2014 May.
Article en En | MEDLINE | ID: mdl-24631179
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.
Asunto(s)
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neumonía / Bronquios / Vasos Linfáticos / Linfangiogénesis / Tejido Linfoide Tipo de estudio: Risk_factors_studies Límite: Animals / Humans Idioma: En Revista: Am J Pathol Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neumonía / Bronquios / Vasos Linfáticos / Linfangiogénesis / Tejido Linfoide Tipo de estudio: Risk_factors_studies Límite: Animals / Humans Idioma: En Revista: Am J Pathol Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos