The clinical manifestations of pulmonary granulomatous diseases are usually the consequence of long-term leukocyte elicitation and activation, resulting in chronic tissue inflammation and lung injury (1). Most interstitial granulomatous diseases in the lung are difficult to treat, requiring therapies that may seriously compromise the immunologic and physiologic integrity of the patient. Historically, the therapeutic approach to the treatment of infectious granulomatous disease has been to target the known infectious agent, while treatment of idiopathic granulomatous diseases has usually targeted immune/inflammatory cell function. Once the pulmonary disease is diagnosed, antimicrobial agents are used to treat the former, while immunosuppressive agents are usually used to treat the latter disease states (2,3). Unfortunately, the clinical management of these diseases does not necessarily ablate the subsequent pathology, which is observed in certain patients. This is especially true in difficult clinical cases, such as drug-resistant mycobacterial diseases or progressive sarcoidosis refractory to corticosteroids (2). Thus, the limited therapeutic options, which are available to effectively manage patients with granulomatous lung disease, may reflect the limited understanding of the mechanisms underlying these chronic diseases.
|Title of host publication||Chemokines in the Lung|
|Number of pages||17|
|Publication status||Published - Jan 1 2003|
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