Wennerås C, Ave P, Huerre M, Arondel J, Ulevitch R J, Mathison J C, Sansonetti P
Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale, Unité 389, Institut Pasteur, Paris, France.
J Immunol. 2000 Mar 15;164(6):3214-21. doi: 10.4049/jimmunol.164.6.3214.
Shigella is a diarrheal pathogen that causes disease through invasion of the large intestinal mucosa. The endotoxin of the invading bacterium may play a key role in the disease process by causing inflammation and tissue injury during infection. Earlier studies have shown that various animal species lacking functional CD14 were protected against endotoxin-mediated shock. Rabbits experimentally infected with Shigella were used to test the hypothesis that blockade of endotoxin-induced cell activation with anti-CD14 mAb would diminish inflammation and thus disease severity. Unexpectedly, we observed that the intestinal mucosa of anti-CD14-treated animals exhibited a 50-fold increase in bacterial invasion and more severe tissue injury compared with controls. Despite higher bacterial loads in treated animals, the numbers of polymorphonuclear leukocytes that were recruited to the infection site were similar to those in controls. Furthermore, the phagocytic cells of CD14-blocked animals produced IL-1 and TNF-alpha. Moreover, in vitro blockade of CD14 did not impede bactericidal activity. Thus, anti-CD14 treatment interfered with host defense mechanisms involved with removal/eradication of Shigella.
志贺氏菌是一种通过侵袭大肠黏膜引发疾病的腹泻病原体。入侵细菌的内毒素可能在疾病进程中起关键作用,它在感染期间会引发炎症和组织损伤。早期研究表明,缺乏功能性CD14的多种动物可免受内毒素介导的休克影响。用实验性感染志贺氏菌的兔子来检验这样一个假说:用抗CD14单克隆抗体阻断内毒素诱导的细胞活化会减轻炎症,进而降低疾病严重程度。出乎意料的是,我们观察到,与对照组相比,接受抗CD14治疗的动物的肠黏膜细菌侵袭增加了50倍,且组织损伤更严重。尽管治疗组动物的细菌载量更高,但募集到感染部位的多形核白细胞数量与对照组相似。此外,CD14阻断动物的吞噬细胞会产生白细胞介素-1和肿瘤坏死因子-α。而且,体外阻断CD14并不妨碍杀菌活性。因此,抗CD14治疗干扰了与志贺氏菌清除相关的宿主防御机制。