Novel @entity19 model of chronic granulomatous lung inflammation elicited by XXXX nanotubes.

@entity1 @entity32 @entity738 @entity19 @entity281 @entity358 @entity1096 @entity74 @entity505
Lung @entity738 are associated with numerous conditions, including inflammatory disorders, exposure to environmental pollutants, and @entity281 . @entity1096 is a chemotactic cytokine produced by macrophages, and is implicated in extracellular matrix remodeling. Furthermore, @entity1096 is up-regulated in @entity738 , and @entity1096 null @entity19 exhibit reduced @entity738 formation. Animal models currently used to investigate chronic lung @entity32 bear a pathological resemblance, but lack the chronic nature of @entity1 @entity738 . @entity505 nanoparticles are generated as byproducts of combustion. Interestingly, experimental exposures to @entity505 nanoparticles induce @entity358 . However, the recruited cellular populations and extracellular matrix gene expression profiles within these lesions have not been explored. Because of the rapid resolution of @entity738 in current animal models, the mechanisms responsible for persistence have been elusive. To overcome the limitations of previous models, we investigated whether a model using multiwall @entity505 nanoparticles would resemble chronic @entity1 lung @entity32 . We hypothesized that pulmonary exposure to multiwall @entity505 nanoparticles would induce @entity738 , elicit a macrophage and T-cell response, and mimic other @entity74 with an up-regulation of @entity1096 . This model demonstrates: (1) @entity32 , with macrophage and T-cell infiltration; (2) resemblance to the chronicity of @entity1 @entity738 , with persistence up to 90 days; and (3) a marked elevation of @entity1096 , metalloproteinases, and cell adhesion molecules in granulomatous foci isolated by laser-capture microdissection and in alveolar macrophages from bronchoalveolar lavage. The establishment of such a model provides an important platform for mechanistic studies on the persistence of @entity738 .
