Cellular and molecular aspects of granulomatous inflammation

Recent advances in cellular and molecular biology have provided important new avenues to assess mechanisms of granuloma formation/regulation. For example, current studies have identified various cytokines that can exert a powerful influence on both immune and non-immune cells and dictate inflammatory processes. Some of these cytokines are potentially active during the initiation and maintenance of chronic inflammation, including tumor necrosis factor, interleukin 1, and a novel class of chemotactic cytokines. This latter group of mediators belongs to a super-gene family of immune signals that play a key role in the selective recruitment of inflammatory cells to an area of inflammation. The coordinated synthesis of these cytokines is likely important to the development of the granulomatous response. The participation of molecular signals produced by non-inflammatory cells, fibroblasts, and epithelial cells, also warrants special consideration. These "bystander" cells appear to possess effector cell functions and likely serve an important role in inducing pulmonary granulomatous inflammation. Thus, a clear understanding of the cells and molecular signals involved in the initiation and maintenance of chronic pulmonary inflammation will be necessary to assess lesion development and design more selective/effective therapies.