Kunkel S L, Lukacs N W, Strieter R M, Chensue S W
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602, USA.
Semin Respir Infect. 1998 Sep;13(3):221-8.
The pathogenesis of granulomatous inflammation is often characterized as an intense inflammatory response with accompanying fibroproliferation and deposition of extracellular matrix. Many of these chronic disorders share a number of common characteristics, including an enigmatic cause, unknown mechanisms of initiation and maintenance, and often untreatable end-stage fibrosis. Granulomatous inflammation can occur in a variety of diseases, such as tuberculosis, sarcoidosis, berylliosis, and Wegner's granulomatosis. Unfortunately, these diseases are often associated with substantial morbidity and mortality, as therapeutic options may not be entirely efficacious. The lack of a clear treatment strategy may underscore the limited scientific understanding of these disorders. Thus, experimental models of granulomatous inflammation, which mimic some of the specific characteristics of these responses, will be useful in delineating the mechanisms of granuloma development. In addition, these models may aid in the design of useful therapies for the treatment of these inflammatory diseases.
肉芽肿性炎症的发病机制通常表现为强烈的炎症反应,并伴有纤维组织增生和细胞外基质沉积。许多这类慢性疾病具有一些共同特征,包括病因不明、起始和维持机制未知,以及终末期纤维化往往难以治疗。肉芽肿性炎症可发生于多种疾病,如结核病、结节病、铍中毒和韦格纳肉芽肿病。不幸的是,这些疾病常常伴随着较高的发病率和死亡率,因为治疗选择可能并不完全有效。缺乏明确的治疗策略可能凸显了对这些疾病的科学认识有限。因此,模拟这些反应某些特定特征的肉芽肿性炎症实验模型,将有助于阐明肉芽肿形成的机制。此外,这些模型可能有助于设计治疗这些炎症性疾病的有效疗法。