Recombinant interleukin-1 stimulates clearance of Escherichia coli K1 bacteraemia.
Enhancement of non-specific resistance to neonatal Escherichia coli K1 infection by interleukin-1 (IL-1) was analysed. Recombinant human IL-1 administered prophylactically to newborn LPS-non-responsive C3H/HeJ mice induced rapid clearance of E. coli 018:K1 bacteraemia. The effect was dose-dependent and was observed with mice treated immediately to 1 day before bacterial challenge, whereas treatment 2 days before challenge was ineffective. was ineffective. Clearance of intravenously injected radiolabelled 018:K1 E. coli suggested that IL-1 triggered defence mechanisms that contribute to bacterial sequestration and killing in the spleen and liver. Comparable increase in bacterial clearance occurred in naturally resistant LPS-responsive mice that had been subjected to transient E. coli K1 bacteraemia and showed increased resistance to reinfection. In the course of E. coli K1 bacteraemia a strong synthesis of acute phase reactants was observed in both susceptible and resistant mouse strains, which indicated that these proteins alone cannot confer natural resistance to E. coli K1. IL-1 induced a very rapid synthesis of acute phase proteins. The clearance of K1 E. coli when still viable in IL-1-treated animals suggested that acute phase proteins are not likely to be major mediators of the IL-1-enhanced non-specific resistance.
Pelkonen
S
S
Basel Institute for Immunology, Switzerland.
Pluschke
G
G
D000209:Acute-Phase Proteins / Q000096:biosynthesis; D000818:Animals; D004927:Escherichia coli Infections / Q000276:immunology*; D007113:Immunity, Innate / Q000187:drug effects; D007375:Interleukin-1 / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D011994:Recombinant Proteins / Q000494:pharmacology; D018805:Sepsis / Q000276:immunology*
D000209:Acute-Phase Proteins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011994:Recombinant Proteins