Granulomatous inflammation of the lung is characterized by the recruitment and organization of activated macrophages and lymphocytes in discrete lesions laced in a network of matrix proteins. These lesions, termed granulomas, represent an important defense mechanism against infectious organisms such as fungi and mycobacteria, but also can be elicited by noninfectious agents. Occasionally, this inflammatory reaction can develop for unknown reasons, causing a systemic illness termed sarcoidosis. The mechanisms involved in granuloma formation in the lung have not been elucidated entirely. However, studies performed in animal models of granuloma formation and in humans suggest important roles for specific soluble mediators (eg, cytokines, chemokines) produced by monocytic cells. If uncontrolled, granulomatous inflammation leads to excessive tissue remodeling, causing fibrosis and/or cavitation as seen in tuberculosis. This review summarizes our current understanding of the factors involved in granuloma formation in the lung with particular attention to their role in sarcoidosis and tuberculosis.
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