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Exogenous cytokine modulation or neutralization of interleukin‐10 enhance survival in lipopolysaccharide‐hyporesponsive C3H/HeJ mice with Klebsiella infection
Author(s) -
M.-J. Wang,
Kee-Ching Jeng,
Ling-In Ping
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00838.x
Subject(s) - lipopolysaccharide , klebsiella pneumoniae , cytokine , tumor necrosis factor alpha , antibody , neutralization , interleukin , microbiology and biotechnology , ratón , biology , lethal dose , immunology , interleukin 6 , escherichia coli , biochemistry , gene , toxicology
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% (LD 50 ) 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 LD 50 infection in C3H/HeJ mice.