VAN DER Meer Jos W M, Vogels Maria T E, Netea Mihai G, Kullberg Bart Jan
Department of Medicine, University Hospital Nijmegen, Nijmegen, The Netherlands.
Ann N Y Acad Sci. 1998 Sep 29;856:243-251. doi: 10.1111/j.1749-6632.1998.tb08331.x.
Bacterial infections in the immunocompromised host cause considerable mortality, and even recently developed antimicrobial strategies often fail to cure these infections, especially in granulocytopenic patients. Cytokines and hematopoietic growth factors have been shown to stimulate host defense mechanisms in vitro and in vivo. The possible role of the proinflammatory cytokines interleukin (IL)-1, tumor necrosis factor-alpha, IL-6, and IL-8 as modulators of host resistance to bacterial infections is discussed. Interleukin-1 has been effective in various animal models of potentially lethal bacterial infection, even during severe granulocytopenia. The protective mechanism of IL-1 may be mediated by downregulation of cytokine receptors and cytokine production and induction of acute phase proteins. Moreover, in subacute and chronic infections IL-1 interferes with microbial outgrowth via mechanisms that have only been partly elucidated.
免疫功能低下宿主中的细菌感染会导致相当高的死亡率，即使是最近开发的抗菌策略也常常无法治愈这些感染，尤其是在粒细胞减少的患者中。细胞因子和造血生长因子已被证明在体外和体内均可刺激宿主防御机制。本文讨论了促炎细胞因子白细胞介素（IL）-1、肿瘤坏死因子-α、IL-6和IL-8作为宿主抵抗细菌感染调节剂的可能作用。白细胞介素-1在各种潜在致命细菌感染的动物模型中均有效，即使在严重粒细胞减少期间也是如此。IL-1的保护机制可能是通过下调细胞因子受体和细胞因子产生以及诱导急性期蛋白来介导的。此外，在亚急性和慢性感染中，IL-1通过仅部分阐明的机制干扰微生物的生长。
