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Research Article Free access | 10.1172/JCI110056
Department of Internal Medicine, University of Texas Health Science Center at Dallas, Texas 75235
Department of Biochemistry, University of Texas Health Science Center at Dallas, Texas 75235
Department of Obstetrics-Gynecology, University of Texas Health Science Center at Dallas, Texas 75235
Department of Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Health Science Center at Dallas, Texas 75235
Find articles by Hurd, E. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Health Science Center at Dallas, Texas 75235
Department of Biochemistry, University of Texas Health Science Center at Dallas, Texas 75235
Department of Obstetrics-Gynecology, University of Texas Health Science Center at Dallas, Texas 75235
Department of Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Health Science Center at Dallas, Texas 75235
Find articles by Johnston, J. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Health Science Center at Dallas, Texas 75235
Department of Biochemistry, University of Texas Health Science Center at Dallas, Texas 75235
Department of Obstetrics-Gynecology, University of Texas Health Science Center at Dallas, Texas 75235
Department of Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Health Science Center at Dallas, Texas 75235
Find articles by Okita, J. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Health Science Center at Dallas, Texas 75235
Department of Biochemistry, University of Texas Health Science Center at Dallas, Texas 75235
Department of Obstetrics-Gynecology, University of Texas Health Science Center at Dallas, Texas 75235
Department of Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Health Science Center at Dallas, Texas 75235
Find articles by MacDonald, P. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Health Science Center at Dallas, Texas 75235
Department of Biochemistry, University of Texas Health Science Center at Dallas, Texas 75235
Department of Obstetrics-Gynecology, University of Texas Health Science Center at Dallas, Texas 75235
Department of Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Health Science Center at Dallas, Texas 75235
Find articles by Ziff, M. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Health Science Center at Dallas, Texas 75235
Department of Biochemistry, University of Texas Health Science Center at Dallas, Texas 75235
Department of Obstetrics-Gynecology, University of Texas Health Science Center at Dallas, Texas 75235
Department of Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Health Science Center at Dallas, Texas 75235
Find articles by Gilliam, J. in: JCI | PubMed | Google Scholar
Published February 1, 1981 - More info
Female B/W mice spontaneously develop an autoimmune disease that is similar to systemic lupus erythematosus. Antibodies to doublestranded DNA (dsDNA) and antinuclear antibodies develop in aging animals; death from immune complex-mediated glomerulonephritis occurs from 8 to 12 mo of age. It has been reported that prostaglandin (PG)E1 treatment of such mice prolongs survival. In the present study, four groups of female B/W mice were studied beginning at 6-11 wk of age on the following regimens: (a) a synthetic diet that contained 20% safflower oil, (b) a standard laboratory chow diet, (c) a standard diet together with injections of PGE1, and (d) an essential fatty acid-deficient synthetic diet that contained 20% coconut oil. All animals were tested monthly for antinuclear antibodies and anti-dsDNA. Kidney tissue was obtained for light and immunofluorescence microscopy when animals were dying. All disease manifestations were altered strikingly in the essential fatty acid (EFA)-deficient animals. Intermediate benefit was seen in PGE1-treated animals. 7% of the control animals and 18% of safflower oil-fed animals survived to 10 mo. In contrast, the PGE1-treated and EFA-deficient mice had a similar survival rate (78-88%). At age 16 mo, 78% of EFA-deficient mice and 45% of PGE1-treated mice were alive. 25% of the PGE1-treated and 55% of the EFA-deficient animals survived to 20 mo. Serum anti-dsDNA appeared at age 5 mo in safflower oil-fed and control animals, but not until 9 and 12 mo for PGE1-treated and EFA-deficient animals, respectively. All kidneys from 7- to 9-mo-old safflower oil-fed and control animals and the majority of kidneys from PGE1-treated animals were abnormal by light and immunofluorescence microscopy. Kidneys from EFA-deficient animals were essentially normal at 10 mo. At 13 mo, all PGE1-treated animals examined had significant kidney involvement, whereas none of the EFA-deficient animals had glomerulonephritis. These findings demonstrate that an EFA-deficient diet has a beneficial effect on murine lupus erythematosus.
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