Increased lipopolysaccharide-induced tumour necrosis factor levels and death in hypercholesterolaemic rabbits.
Journal: 1995/September - Clinical and Experimental Immunology
ISSN: 0009-9104
PUBMED: 7648721
Abstract:
Nutritional-induced hypercholesterolaemia in New Zealand rabbits causes increased susceptibility to experimental infections. Rabbits fed cholesterol (0.5 g%) for 8 weeks were injected intravenously with varying doses of Escherichia coli 0127: B8 lipopolysaccharide (LPS; 3-100 micrograms/kg). The levels of cholesterol, triglycerides, tumour necrosis factor (TNF), and the survival rates of treated rabbits were then measured. Rabbits fed either normal chow or chow impregnated with sesame oil were used as controls. LPS induced higher serum TNF levels in hypercholesterolaemic rabbits than in normal rabbits or rabbits fed with chow containing sesame oil. TNF levels rose faster in hypercholesterolaemic rabbits than in normal rabbits, reaching maximum levels at 60 min and 120 min, respectively, after LPS injection. The survival rate of hypercholesterolaemic rabbits (1/11) was lower than in normal rabbits (6/7) or rabbits fed with the sesame oil chow (4/4) at the higher LPS doses. No death occurred at lower doses. One possible interpretation of these results, also supported by neutralization experiments, is that increased TNF secretion in hypercholesterolaemic rabbits raises the host's susceptibility to experimental endotoxaemia and possibly to Gram-negative infection.
Relations:
Content
Citations
(3)
References
(35)
Diseases
(1)
Drugs
(1)
Chemicals
(3)
Organisms
(3)
Processes
(1)
Anatomy
(1)
Similar articles
Articles by the same authors
Discussion board
Clin Exp Immunol 101(2): 357-361

Increased lipopolysaccharide-induced tumour necrosis factor levels and death in hypercholesterolaemic rabbits.

Abstract

Nutritional-induced hypercholesterolaemia in New Zealand rabbits causes increased susceptibility to experimental infections. Rabbits fed cholesterol (0.5 g%) for 8 weeks were injected intravenously with varying doses of Escherichia coli 0127: B8 lipopolysaccharide (LPS; 3-100 micrograms/kg). The levels of cholesterol, triglycerides, tumour necrosis factor (TNF), and the survival rates of treated rabbits were then measured. Rabbits fed either normal chow or chow impregnated with sesame oil were used as controls. LPS induced higher serum TNF levels in hypercholesterolaemic rabbits than in normal rabbits or rabbits fed with chow containing sesame oil. TNF levels rose faster in hypercholesterolaemic rabbits than in normal rabbits, reaching maximum levels at 60 min and 120 min, respectively, after LPS injection. The survival rate of hypercholesterolaemic rabbits (1/11) was lower than in normal rabbits (6/7) or rabbits fed with the sesame oil chow (4/4) at the higher LPS doses. No death occurred at lower doses. One possible interpretation of these results, also supported by neutralization experiments, is that increased TNF secretion in hypercholesterolaemic rabbits raises the host's susceptibility to experimental endotoxaemia and possibly to Gram-negative infection.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (883K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Carswell EA, Old LJ, Kassel RL, Green S, Fiore N, Williamson B. An endotoxin-induced serum factor that causes necrosis of tumors. Proc Natl Acad Sci U S A. 1975 Sep;72(9):3666–3670.[PMC free article] [PubMed] [Google Scholar]
  • Raetz CR, Ulevitch RJ, Wright SD, Sibley CH, Ding A, Nathan CF. Gram-negative endotoxin: an extraordinary lipid with profound effects on eukaryotic signal transduction. FASEB J. 1991 Sep;5(12):2652–2660. [PubMed] [Google Scholar]
  • Cerami A, Beutler B. The role of cachectin/TNF in endotoxic shock and cachexia. Immunol Today. 1988 Jan;9(1):28–31. [PubMed] [Google Scholar]
  • Caput D, Beutler B, Hartog K, Thayer R, Brown-Shimer S, Cerami A. Identification of a common nucleotide sequence in the 3'-untranslated region of mRNA molecules specifying inflammatory mediators. Proc Natl Acad Sci U S A. 1986 Mar;83(6):1670–1674.[PMC free article] [PubMed] [Google Scholar]
  • Tartaglia LA, Goeddel DV. Two TNF receptors. Immunol Today. 1992 May;13(5):151–153. [PubMed] [Google Scholar]
  • Dinarello CA. Role of interleukin-1 in infectious diseases. Immunol Rev. 1992 Jun;127:119–146. [PubMed] [Google Scholar]
  • Sherry B, Cerami A. Cachectin/tumor necrosis factor exerts endocrine, paracrine, and autocrine control of inflammatory responses. J Cell Biol. 1988 Oct;107(4):1269–1277.[PMC free article] [PubMed] [Google Scholar]
  • Mathison JC, Wolfson E, Ulevitch RJ. Participation of tumor necrosis factor in the mediation of gram negative bacterial lipopolysaccharide-induced injury in rabbits. J Clin Invest. 1988 Jun;81(6):1925–1937.[PMC free article] [PubMed] [Google Scholar]
  • Adi S, Pollock AS, Shigenaga JK, Moser AH, Feingold KR, Grunfeld C. Role for monokines in the metabolic effects of endotoxin. Interferon-gamma restores responsiveness of C3H/HeJ mice in vivo. J Clin Invest. 1992 May;89(5):1603–1609.[PMC free article] [PubMed] [Google Scholar]
  • Rus HG, Niculescu F, Vlaicu R. Tumor necrosis factor-alpha in human arterial wall with atherosclerosis. Atherosclerosis. 1991 Aug;89(2-3):247–254. [PubMed] [Google Scholar]
  • Fleet JC, Clinton SK, Salomon RN, Loppnow H, Libby P. Atherogenic diets enhance endotoxin-stimulated interleukin-1 and tumor necrosis factor gene expression in rabbit aortae. J Nutr. 1992 Feb;122(2):294–305. [PubMed] [Google Scholar]
  • Libby P, Hansson GK. Involvement of the immune system in human atherogenesis: current knowledge and unanswered questions. Lab Invest. 1991 Jan;64(1):5–15. [PubMed] [Google Scholar]
  • Kos WL, Loria RM, Snodgrass MJ, Cohen D, Thorpe TG, Kaplan AM. Inhibition of host resistance by nutritional hypercholesteremia. Infect Immun. 1979 Nov;26(2):658–667.[PMC free article] [PubMed] [Google Scholar]
  • Fiser RH, Jr, Denniston JC, McGann VG, Kaplan J, Alder WH, 3rd, Kastello MD, Beisel WR. Altered immune function in hypercholesterolemic monkeys. Infect Immun. 1973 Jul;8(1):105–109.[PMC free article] [PubMed] [Google Scholar]
  • Klurfeld DM, Allison MJ, Gerszten E, Dalton HP. Alterations of host defenses paralleling cholesterol-induced atherogenesis. I. Interactions of prolonged experimental hypercholesterolemia and infections. J Med. 1979;10(1-2):35–48. [PubMed] [Google Scholar]
  • Klurfeld DM, Allison MJ, Gerszten E, Dalton HP. Alterations of host defenses paralleling cholesterol-induced atherogenesis. II. Immunologic studies of rabbits. J Med. 1979;10(1-2):49–64. [PubMed] [Google Scholar]
  • Pereira CA, Steffan AM, Koehren F, Douglas CR, Kirn A. Increased susceptibility of mice to MHV 3 infection induced by hypercholesterolemic diet: impairment of Kupffer cell function. Immunobiology. 1987 May;174(3):253–265. [PubMed] [Google Scholar]
  • Brito B, Romano E, Soyano A. Functional characterization of mononuclear cells of normal and hypercholesterolemic rabbits. J Med. 1989;20(3-4):273–285. [PubMed] [Google Scholar]
  • BOWMAN RE, WOLF RC. A rapid and specific ultramicro method for total serum cholesterol. Clin Chem. 1962 May-Jun;8:302–309. [PubMed] [Google Scholar]
  • Biggs HG, Erikson JM, Moorehead WR. A manual colormetric assay of triglycerides in serum. Clin Chem. 1975 Mar;21(3):437–441. [PubMed] [Google Scholar]
  • Espevik T, Nissen-Meyer J. A highly sensitive cell line, WEHI 164 clone 13, for measuring cytotoxic factor/tumor necrosis factor from human monocytes. J Immunol Methods. 1986 Dec 4;95(1):99–105. [PubMed] [Google Scholar]
  • Eskandari MK, Nguyen DT, Kunkel SL, Remick DG. WEHI 164 subclone 13 assay for TNF: sensitivity, specificity, and reliability. Immunol Invest. 1990 Feb;19(1):69–79. [PubMed] [Google Scholar]
  • Beutler B, Greenwald D, Hulmes JD, Chang M, Pan YC, Mathison J, Ulevitch R, Cerami A. Identity of tumour necrosis factor and the macrophage-secreted factor cachectin. Nature. 1985 Aug 8;316(6028):552–554. [PubMed] [Google Scholar]
  • Atherosclerosis goes to the wall. Lancet. 1992 Mar 14;339(8794):647–648. [PubMed] [Google Scholar]
  • Tobias PS, Soldau K, Ulevitch RJ. Isolation of a lipopolysaccharide-binding acute phase reactant from rabbit serum. J Exp Med. 1986 Sep 1;164(3):777–793.[PMC free article] [PubMed] [Google Scholar]
  • Mathison JC, Tobias PS, Wolfson E, Ulevitch RJ. Plasma lipopolysaccharide (LPS)-binding protein. A key component in macrophage recognition of gram-negative LPS. J Immunol. 1992 Jul 1;149(1):200–206. [PubMed] [Google Scholar]
  • Bosch Román V, Arreaza Plaza C, Pieters Osió G, Santana C. Acidos grasos esterificados del plasma en residentes de caracas aparentemente normales y en pacientes que han sufrido un infarto del miocardio. Acta Cient Venez. 1978;29(5):400–403. [PubMed] [Google Scholar]
  • Kunkel SL, Spengler M, May MA, Spengler R, Larrick J, Remick D. Prostaglandin E2 regulates macrophage-derived tumor necrosis factor gene expression. J Biol Chem. 1988 Apr 15;263(11):5380–5384. [PubMed] [Google Scholar]
  • Hardard'ottir I, Whelan J, Kinsella JE. Kinetics of tumour necrosis factor and prostaglandin production by murine resident peritoneal macrophages as affected by dietary n-3 polyunsaturated fatty acids. Immunology. 1992 Aug;76(4):572–577.[PMC free article] [PubMed] [Google Scholar]
  • Fieren MW, van den Bemd GJ, Ben-Efraim S, Bonta IL. Prostaglandin E2 inhibits the release of tumor necrosis factor-alpha, rather than interleukin 1 beta, from human macrophages. Immunol Lett. 1992 Jan;31(1):85–90. [PubMed] [Google Scholar]
  • Harris HW, Grunfeld C, Feingold KR, Rapp JH. Human very low density lipoproteins and chylomicrons can protect against endotoxin-induced death in mice. J Clin Invest. 1990 Sep;86(3):696–702.[PMC free article] [PubMed] [Google Scholar]
  • Harris HW, Grunfeld C, Feingold KR, Read TE, Kane JP, Jones AL, Eichbaum EB, Bland GF, Rapp JH. Chylomicrons alter the fate of endotoxin, decreasing tumor necrosis factor release and preventing death. J Clin Invest. 1993 Mar;91(3):1028–1034.[PMC free article] [PubMed] [Google Scholar]
  • Van Lenten BJ, Fogelman AM, Haberland ME, Edwards PA. The role of lipoproteins and receptor-mediated endocytosis in the transport of bacterial lipopolysaccharide. Proc Natl Acad Sci U S A. 1986 Apr;83(8):2704–2708.[PMC free article] [PubMed] [Google Scholar]
  • Flegel WA, Wölpl A, Männel DN, Northoff H. Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins. Infect Immun. 1989 Jul;57(7):2237–2245.[PMC free article] [PubMed] [Google Scholar]
  • Baumberger C, Ulevitch RJ, Dayer JM. Modulation of endotoxic activity of lipopolysaccharide by high-density lipoprotein. Pathobiology. 1991;59(6):378–383. [PubMed] [Google Scholar]
Pathophysiology Laboratory, Venezuelan Institute for Scientific Research (IVIC), Caracas.
Pathophysiology Laboratory, Venezuelan Institute for Scientific Research (IVIC), Caracas.
Abstract
Nutritional-induced hypercholesterolaemia in New Zealand rabbits causes increased susceptibility to experimental infections. Rabbits fed cholesterol (0.5 g%) for 8 weeks were injected intravenously with varying doses of Escherichia coli 0127: B8 lipopolysaccharide (LPS; 3-100 micrograms/kg). The levels of cholesterol, triglycerides, tumour necrosis factor (TNF), and the survival rates of treated rabbits were then measured. Rabbits fed either normal chow or chow impregnated with sesame oil were used as controls. LPS induced higher serum TNF levels in hypercholesterolaemic rabbits than in normal rabbits or rabbits fed with chow containing sesame oil. TNF levels rose faster in hypercholesterolaemic rabbits than in normal rabbits, reaching maximum levels at 60 min and 120 min, respectively, after LPS injection. The survival rate of hypercholesterolaemic rabbits (1/11) was lower than in normal rabbits (6/7) or rabbits fed with the sesame oil chow (4/4) at the higher LPS doses. No death occurred at lower doses. One possible interpretation of these results, also supported by neutralization experiments, is that increased TNF secretion in hypercholesterolaemic rabbits raises the host's susceptibility to experimental endotoxaemia and possibly to Gram-negative infection.
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.