Indexé dans
  • Ouvrir la porte J
  • Genamics JournalSeek
  • Clés académiques
  • JournalTOCs
  • RechercheBible
  • Infrastructure nationale des connaissances en Chine (CNKI)
  • Scimago
  • Répertoire des périodiques d'Ulrich
  • Bibliothèque des revues électroniques
  • RechercheRef
  • Université Hamdard
  • EBSCO AZ
  • OCLC - WorldCat
  • Catalogue en ligne SWB
  • Bibliothèque virtuelle de biologie (vifabio)
  • Publions
  • MIAR
  • Services d'indexation scientifique (SIS)
  • Pub européen
  • Google Scholar
Partager cette page
Dépliant de journal
Flyer image

Abstrait

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.