Exogenous cytokine modulation or neutralization of interleukin‐10 enhance survival in lipopolysaccharide‐hyporesponsive C3H/HeJ mice with Klebsiella infection
Exogenous cytokine modulation or neutralization of interleukin‐10 enhance survival in lipopolysaccharide‐hyporesponsive C3H/HeJ mice with Klebsiella infection
复制标题
外源细胞因子调节或中和白细胞介素 10 可提高克雷伯氏菌感染的脂多糖低反应性 C3H/HeJ 小鼠的存活率
作者:
Wang;Jeng;Ping
Klebsiella pneumoniae has been isolated from liver abscesses in patients with leukaemia or diabetes. The resistance of Klebsiella infection in lipopolysaccharide (LPS)‐hyporesponsive mice is unclear. Female C3H/HeJ and C3H/HeN mice, 6–8 weeks old, were intraperitoneally (i.p.) injected with K. pneumoniae. The results showed that C3H/HeJ mice were 24 times more susceptible [lethal dose 50% (LD50) 250 colony‐forming units] than C3H/HeN mice to K. pneumoniae infection. C3H/HeJ mice, uninfected or infected with K. pneumoniae, had higher liver interleukin (IL)‐10 levels and IL‐10 mRNA levels than C3H/HeN mice. Previously, pretreatment with IL‐1β and tumour necrosis factor‐α (TNF‐α) protected C3H/HeJ mice from lethal bacterial infection. Therefore the effects of pretreatment with IL‐1β and TNF‐α or antimurine IL‐10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. Pretreatment with TNF‐α or anti‐IL‐10 antibody enhanced the survival of both strains of mice. TNF‐α, in combination with IL‐1β, enhanced the survival and bacterial clearance better than single pretreatment in C3H/HeJ mice. Anti‐IL‐10 antibody increased bacterial clearance and significantly reduced liver cytokine mRNA levels in C3H/HeJ mice more than it did in the controls during infection. These results indicate that exogenous cytokine modulation or neutralization of IL‐10 enhance the resistance of LD50 infection in C3H/HeJ mice.
DOI:
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发表时间:
1985
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Hagberg,L;Briles,DE;Eden,CS
通讯作者:
Eden,CS
影响因子:
4.3
作者:
Weinstein,DL;Lissner,CR;Swanson,RN;O'Brien,AD
通讯作者:
O'Brien,AD
影响因子:
4.4
作者:
M. Greenberger;R. Strieter;S. Kunkel;J. Danforth;R. Goodman;T. Standiford
通讯作者:
M. Greenberger;R. Strieter;S. Kunkel;J. Danforth;R. Goodman;T. Standiford