Animal models of chronic lung disease

Information derived from a variety of experimental animal models suggests that a number of cytokines play a role in the initiation, maintenance, and resolution of chronic interstitial pulmonary inflammation. However, the mechanism by which each cytokine is involved in the evolution of the inflammatory response is not clear. For example, in vivo studies assessing the development of interstitial lung granulomas induced by a mycobacterial antigen, purified protein derivative (PPD), have demonstrated that IFN-y and TNF were necessary cytokines for lesion progression (52). In contrast, pulmonary inflammation initiated by either the 

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A novel aspect of these experiments was the use of in vivo model systems, which express a cytokine profile consistent with either a Thl- or Th2-type response. We have utilized an experimental pulmonary granuloma model, which begins as a primary, Thl response, and naturally evolves into a response with Th2-type characteristics (52-54). This system allows for the assessment of the temporal expression pattern of chemokines and chemokine receptors and the mediator systems that are responsible for the expression of these ligands and receptors. 

In initial studies we measured the levels of CXCLIO and CXCL9 in the lung of both normal animals and animals with developing Thl-type granulomas. 

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