indexado en
  • Abrir puerta J
  • Genamics JournalSeek
  • Claves Académicas
  • DiarioTOCs
  • InvestigaciónBiblia
  • Infraestructura Nacional de Conocimiento de China (CNKI)
  • cimago
  • Directorio de publicaciones periódicas de Ulrich
  • Biblioteca de revistas electrónicas
  • Búsqueda de referencia
  • Universidad Hamdard
  • EBSCO AZ
  • OCLC-WorldCat
  • Catálogo en línea SWB
  • Biblioteca Virtual de Biología (vifabio)
  • Publón
  • miar
  • Servicios de indexación científica (SIS)
  • pub europeo
  • Google Académico
Comparte esta página
Folleto de diario
Flyer image

Abstracto

Exposure to a Mycobacterial Antigen, ESAT-6, Exacerbates Granulomatous and Fibrotic Changes in a Multiwall Carbon Nanotube Model of Chronic Pulmonary Disease

Anagha Malur, Barbara P Barna, Janki Patel, Matthew McPeek, Christopher J Wingard, Larry Dobbs and Mary Jane Thomassen

Recent studies suggest additive effects of environmental pollutants and microbial antigens on respiratory disease. We established a granuloma model in which instilled multiwall carbon nanotubes (MWCNT) elicit granulomatous pathology. We hypothesized that mycobacterial antigen ESAT-6, a T cell activator associated with tuberculosis and sarcoidosis, might alter pathology. Wild-type C57Bl/6 mice received MWCNT with or without ESAT-6 peptide. Controls received vehicle (surfactant-PBS) or ESAT-6 alone. Mice were evaluated 60 days later for granulomas, fibrosis, and bronchoalveolar lavage (BAL) cell expression of inflammatory mediators (CCL2, MMP-12, and Osteopontin). Results indicated increased granulomas, fibrosis, and inflammatory mediators in mice receiving the combination of MWCNT+ESAT-6 compared to MWCNT or vehicle alone. ESAT-6 alone showed no significant effect on these pathological endpoints. However, CD3 (+) lymphocyte infiltration of lung tissue increased with MWCNT+ESAT-6 versus MWCNT alone. Findings suggest that concurrent exposure to microbial antigen and MWCNT exacerbates chronic pulmonary disease.