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      Thermal Response to Zymosan: The Differential Role of Complement

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      S. Karger AG

      Fever, Guinea pigs, Cobra venom factor, Innate immunity

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          Objectives: This study was designed to determine whether the complement (C) system may be involved in the febrile response to zymosan (Zym), a glycan derived from yeast cell walls. Methods: Cobra venom factor (CVF) at 100 U/animal or its vehicle, pyrogen-free saline (PFS), was injected intravenously (i.v.) into guinea pigs to deplete serum C. Eighteen hours later, a low or high dose of Zym or its vehicle, PFS, was administered i.v. or intraperitoneally (i.p.) to these animals. The core temperature (T<sub>c</sub>) was measured continuously by thermocouples. Serum C levels were determined by sheep erythrocyte hemolytic assay. Results: Zym at 1 mg/kg caused a 1°C T<sub>c</sub> rise that was not significantly affected by CVF pretreatment. However, CVF-induced hypocomplementation converted the T<sub>c</sub> fall (∼1.2°C) produced by 100 mg/kg of Zym i.p. into a 1°C T<sub>c</sub> rise. Similarly, CVF pretreatment did not affect the T<sub>c</sub> rise caused by 0.5 mg/kg of Zym i.v., but converted the T<sub>c</sub> fall induced by 25 mg/kg i.v. into a 1°C T<sub>c</sub> rise. A separate experiment showed that 25, but not 0.5 mg/kg of Zym i.v., decreased serum C by 34% in 15 min; C did not recover over the next 6 h. A second i.v. injection of 25 mg Zym/kg 210 min later, when the T<sub>c</sub> had recovered but the serum C had not, yielded a smaller and briefer T<sub>c</sub> fall. Conclusion: These results suggest that Zym is inherently pyrogenic, but this effect is manifested only when the dose of zymosan is too small to activate C or when C has been reduced by prior activation.

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          Most cited references 2

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          Molecular mechanism of tumor necrosis factor-alpha production in 1-->3-beta-glucan (zymosan)-activated macrophages.

          The molecular details of 1-->3-beta-glucans, a fungal cell wall component, induced inflammatory responses are not well understood. In the present study, we conducted a systematic analysis of the molecular events leading to tumor necrosis factor (TNF)-alpha production after glucan stimulation of macrophages. We demonstrated that activation of nuclear factor kappaB (NF-kappaB) is essential in zymosan A (a source of 1-->3-beta-glucans)-induced TNF-alpha production in macrophages (RAW264.7 cells). Zymosan A-induced TNF-alpha protein production was associated with an increase in the TNF-alpha gene promoter activity. Activation of the TNF-alpha gene promoter was dependent on activation of NF-kappaB. Time course studies indicated that DNA binding activity of NF-kappaB preceded TNF-alpha promoter activity. Inhibition of NF-kappaB activation led to a dramatic reduction in both TNF-alpha promoter activity and TNF-alpha protein production in the response to zymosan A. Mutation of a major NF-kappaB binding site (kappa3) in the gene promoter resulted in a significant decrease in the induction of the gene promoter by zymosan A, while mutation of Egr or CRE sites failed to inhibit the response to zymosan. Together, these results strongly suggest that NF-kappaB is involved in signal transduction of 1-->3-beta-glucans-induced TNF-alpha expression.
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            Modulation of mouse endotoxic fever by complement

             S. Li,  V. Holers,  S. Boackle (2002)

              Author and article information

              S. Karger AG
              October 2002
              04 October 2002
              : 10
              : 2
              : 122-128
              Department of Physiology, University of Tennessee Health Science Center, Memphis, Tenn., USA
              65187 Neuroimmunomodulation 2002–03;10:122–128
              © 2002 S. Karger AG, Basel

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              Figures: 4, References: 25, Pages: 7
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