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Cytokine-Networks and ARDS

1997; Springer Nature; Linguagem: Inglês

10.1007/978-3-662-13450-4_8

0942-5381

P. G. Jorens, Leo Bossaert,

Sepsis Diagnosis and Treatment

The acute respiratory distress syndrome (ARDS), a process of non-hydrostatic pulmonary edema and hypoxemia with a variety of etiologies, consists of diffuse, acute parenchymal lung injury that results in increased permeability and mechanical dysfunction [1]. In recent years, a large body of research has focused on a key role for polymorphonuclear leukocytes (PMN) in the pathogenesis of ARDS. Recently, interest has shifted from formed blood elements to both the alveolar macrophage, the resident phagocyte of the alveolar space, and cytokines. In this hypothesis, ARDS is related to the uncontrolled production and liberation of many substances, including cytokines. Cytokines are low-molecular weight proteins, arbitrarily divided into several classes: interleukins (originally described as messengers between leukocytes), interferons (named after their ability to interfere in the life cycle of viruses), growth factors, colony-stimulating factors and chemokines. However, most cytokines are pleiotropic and have multiple, diverse, biological activities [2], frequently not related to their original name.