van der Meer J W, Vogels M T, Kullberg B J
Department of Medicine, University Hospital Nijmegen, The Netherlands.
Biotherapy. 1994;7(3-4):161-7. doi: 10.1007/BF01878482.
Bacterial infections in the immunocompromized host cause considerable mortality, and even the 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. We discuss the possible role of the pro-inflammatory cytokines interleukin-1, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 as modulators of host resistance to bacterial infections. Interleukin-1 has been shown effective in various animal models of potentially lethal bacterial infection, even during severe granulocytopenia. The protective mechanism of interleukin-1 may be mediated via downregulation of cytokine receptors and cytokine production, and via induction of acute phase proteins. Moreover, in subacute and chronic infections interleukin-1 interferes with microbial outgrowth, via mechanisms that have only been partially 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。我们讨论了促炎细胞因子白细胞介素-1、肿瘤坏死因子-α、白细胞介素-6和白细胞介素-8作为宿主抵抗细菌感染的调节因子的可能作用。白细胞介素-1已被证明在各种潜在致命细菌感染的动物模型中有效，即使在严重粒细胞减少期间也是如此。白细胞介素-1的保护机制可能通过细胞因子受体和细胞因子产生的下调以及急性期蛋白的诱导来介导。此外，在亚急性和慢性感染中，白细胞介素-1通过仅部分阐明的机制干扰微生物的生长。
