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Differential Susceptibility to Lethal Endotoxemia in Mice Deficient in IL-1alpha, IL-1beta or IL-1 Receptor Type I.

NETEA MG, VONK AG, BOERMAN O, JOOSTEN LA, KULLBERG BJ, VAN DER MEER JW; Interscience Conference on Antimicrobial Agents and Chemotherapy (43rd: 2003: Chicago, Ill.).

Abstr Intersci Conf Antimicrob Agents Chemother Intersci Conf Antimicrob Agents Chemother. 2003 Sep 14-17; 43: abstract no. B-1507.

University Medical Center Nijmegen, Nijmegen, Netherlands.

BACKGROUND: Controversial data are available regarding the role of endogenous intereukin-1 (IL-1) in the mortality due to endotoxemia. We investigated the role of IL-1 in lethal endotoxemia in mice deficient in either IL-1a , IL-1b or IL-1 receptor type I (IL-1RI). METHODS: IL-1a -/-, IL-1b -/-, IL-1RI-/- and control mice were injected i.v. with Escherichia coli LPS (0.25 to 1.0 mg/mouse). Cytokine circulating levels were measured 90 min and 3h after LPS, with survival assessed daily. The kinetics of IL-1a clearance was investigated by i.v. challenge with radioactive [125]I-IL-1a . The expression of IL-1RI and IL-1R accesory protein (IL-1RAcP) in the tissues was measured by quantitative RT-PCR. RESULTS: IL-1b -/- mice were normally susceptible to lethal endotoxaemia, and IL-1a and TNF production did not differ to that in control mice. Surprisingly, when IL-1a -/- mice were challenged with a sublethal LPS dose (0.25 mg), the mortality was higher than that in control mice (90% vs. 10%, p<0.01). The hypothesis that this effect was due to a distorted homeostasis of IL-1RI receptor-mediated pathways was sustained by a strongly decreased clearance of radioactive [125]I-IL-1 injected i.v. into IL-1a -/- mice. A distorted homeostasis of the IL-1 receptors in the tissues of the IL-1a -/- mice was in line with the 40 to 65% reduction of the expression of IL-1RI and IL-1RAcP in the peritoneal macrophages of IL-1a -/- mice. In contrast to the IL-1a -/- and IL-1b -/- mice, IL-1RI-/- mice were completely resistant (0% mortality) when challenged with lethal doses of 1.0 mg LPS (mortality in the control mice 90%, p<0.01). CONCLUSIONS: IL-1RI-mediated signals are crucial in mediating mortality due to lethal endotoxemia. Investigation of IL-1-mediated pathways in IL-1-/- mice is complicated by a distorted homeostasis of IL-1RI and IL-1RAcP expression, resulting in a modified IL-1 clearance, making them less suited for the study of IL-1 effects in experimental models.

Publication Types:
  • Meeting Abstracts
Keywords:
  • Animals
  • Carrier Proteins
  • Cytokines
  • Disease Susceptibility
  • Endotoxemia
  • Interleukin-1
  • Interleukin-1 Receptor Accessory Protein
  • Interleukin-1beta
  • Lipopolysaccharides
  • Macrophages, Peritoneal
  • Mice
  • Mice, Inbred C57BL
  • Muridae
  • Protein Binding
  • Proteins
  • Receptors, Interleukin-1
  • deficiency
  • immunology
Other ID:
  • GWAIDS0025663
UI: 102265287

From Meeting Abstracts




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