革兰氏阴性细菌感染在黏膜表面诱导产生白细胞介素-6。
Interleukin-6 induced at mucosal surfaces by gram-negative bacterial infection.
作者信息
de Man P, van Kooten C, Aarden L, Engberg I, Linder H, Svanborg Edén C
机构信息
Department of Clinical Immunology, University of Göteborg, Sweden.
出版信息
Infect Immun. 1989 Nov;57(11):3383-8. doi: 10.1128/iai.57.11.3383-3388.1989.
Abstract
Interleukin-6 (IL-6) was produced in response to mucosal and systemic infection of mice with gram-negative bacteria. The IL-6 response was controlled by the lipopolysaccharide gene, Lps; in C3H/HeN mice (Lpsn/Lpsn), the urinary IL-6 levels increased within 30 min after challenge with Escherichia coli, but no response occurred in C3H/HeJ mice (Lpsd/Lpsd). In lipopolysaccharide-responder mice, the levels of local and systemic IL-6 were related to the degree of infection. The urinary response dominated after intravesical challenge, and the serum response dominated after intraperitoneal challenge. The results demonstrate that IL-6 is activated as part of lipopolysaccharide-induced mucosal and systemic responses to gram-negative bacterial infections.
摘要
白细胞介素-6（IL-6）是小鼠受到革兰氏阴性菌黏膜感染和全身感染后产生的。IL-6反应受脂多糖基因Lps控制；在C3H/HeN小鼠（Lpsn/Lpsn）中，用大肠杆菌攻击后30分钟内尿IL-6水平升高，但C3H/HeJ小鼠（Lpsd/Lpsd）无反应。在脂多糖反应小鼠中，局部和全身IL-6水平与感染程度相关。膀胱内攻击后尿反应占主导地位，腹腔内攻击后血清反应占主导地位。结果表明，IL-6作为脂多糖诱导的对革兰氏阴性菌感染的黏膜和全身反应的一部分被激活。
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