Exogenous cytokine modulation or neutralization of interleukin-10 enhance survival in lipopolysaccharide-hyporesponsive C3H/HeJ mice with Klebsiella infection

Citation
Mj. Wang et al., Exogenous cytokine modulation or neutralization of interleukin-10 enhance survival in lipopolysaccharide-hyporesponsive C3H/HeJ mice with Klebsiella infection, IMMUNOLOGY, 98(1), 1999, pp. 90-97
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Immunology
Journal title
IMMUNOLOGY
ISSN journal
0019-2805 → ACNP
Volume
98
Issue
1
Year of publication
1999
Pages
90 - 97
Database
ISI
SICI code
0019-2805(199909)98:1<90:ECMONO>2.0.ZU;2-L
Abstract
Klebsiella pneumoniae has been isolated from liver abscesses in patients wi th leukaemia or diabetes. The resistance of Klebsiella infection in lipopol ysaccharide (LPS)-hyporesponsive mice is unclear. Female C3H/HeJ and C3H/He N mice, 6-8 weeks old, were intraperitoneally (i.p.) injected with K. pneum oniae. 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. p neumoniae infection. C3H/HeJ mice, uninfected or infected with K. pneumonia e, had higher liver interleukin (IL)-10 levels and IL-10 mRNA levels than C 3H/HeN mice. Previously, pretreatment with IL-1 beta and tumour necrosis fa ctor-alpha (TNF-alpha) protected C3H/HeJ mice from lethal bacterial infecti on. Therefore the effects of pretreatment with IL-1 beta and TNF-alpha or a ntimurine IL-10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. Pretreatment with TNF-alpha or anti-IL-10 antibody enhanced the survival of both strains of mice. TNF-alpha, in combination w ith IL-1 beta, enhanced the survival and bacterial clearance better than si ngle pretreatment in C3H/HeJ mice. Anti-IL-10 antibody increased bacterial clearance and significantly reduced liver cytokine mRNA levels in C3H/HeJ m ice more than it did in the controls during infection. These results indica te that exogenous cytokine modulation or neutralization of IL-10 enhance th e resistance of LD50 infection in C3H/HeJ mice.