Effect of prostaglandin E1 in brown Norway rats with mercury-induced autoimmune disease

Hinglais, N; Pelletier, Lucette; Vial, M C; Sapin, Catherine; Bascou, C.; Bariéty, J; Kelley, Vicki Rubin; Druet, Philippe

doi:10.1016/0090-1229(86)90184-4

Cited by 9 publications

(2 citation statements)

References 13 publications

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“…Ninety-six-well microtiter plates (Nunc, Kamstrup, Denmark) were coated overnight at 4°C with 100 pl of a solution of BP at 1 pg/ml in PBS. Test sera were diluted M O O in PBS containing 1% bovine serum albumin and 0.1 % Tween 20 and incubated for 90 min at 37 "C. After washing, bound IgG were revealed with peroxidaselabeled sheep IgG anti-rat IgG prepared as described elsewhere [21]. Sera were titrated by comparison with a standard serum pool obtained from LEW rats immunized three times with BP (2 mghnjection) in CFA.…”

Section: Anti-myelin Bp Antibodiesmentioning

confidence: 99%

Effect of HgCl2 on experimental allergic encephalomyelitis in Lewis rats. HgC12i-nduced down-modulation of the disease

et al. 1988

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HgCl2 induces autoimmunity in Brown-Norway rats and immunosuppression in Lewis rats. In the latter rats, HgCl2 triggers the proliferation of T suppressor/cytotoxic (OX8+) cells which actively suppress T cell functions. This led us to study the effect of HgCl2 on experimental allergic encephalomyelitis (EAE), a T cell-mediated autoimmune disease obtained following immunization with basic protein (BP). It will be shown that HgCl2 attenuates or even prevents clinical manifestations of EAE and inhibits both the proliferative response of T cells to BP and the anti-BP antibody response. This immunosuppression was not due to a defect at the T helper cell or antigen-processing cell level but to the emergence of T suppressor cells.

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Section: Anti-myelin Bp Antibodiesmentioning

confidence: 99%

Effect of HgCl2 on experimental allergic encephalomyelitis in Lewis rats. HgC12i-nduced down-modulation of the disease

et al. 1988

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“…For example, TXB2 is a potent vasoconstrictor [27,28] and platelet aggregator agonist [29]. Platelet aggregation is also implicated in glomerular injury [30][31][32][33], TXA2 is also a leukocyte chemoattractant; therefore, the well-known tissue-damaging effects of stim ulated leukocytes could come into play [34,35], The decreased PG production (PGE2, PGH) by CsA facili tated the role of TXA2 and 5-HT, because PG infusion has previously been shown to reduce immune complex autoimmune glomerulonephritis [36][37][38][39] and ARF [13][14][15][16]24], Thus, KTS that was found to increase the ratios of PGE2/TXB2 and 6kPGE|a (PGI2)/TXB2 (table 3) and, furthermore, antagonizes the vasoconstrictor S2 seroton ergic receptors [9], prevents the NT induced by CsA. In conclusion, KTS by antagonizing the vasoconstrictor S2 (mainly) serotonergic, a 1 adrenergic and Hi histaminergic receptors, without affecting the vasodilator S2 serotoner gic receptors [9,25] and by increasing the ratios of PGE2/ TXB2 and 6kPGF|"/TXB2 prevented, at least in part, the NT induced by CsA.…”

Section: Effect O F Csa In Kts-pretreated Ratsmentioning

confidence: 99%

Effect of Ketanserine in Cyclosporine-lnduced Renal Dysfunction in Rats

Darlametsos¹,

Morphake²,

Bariéty

et al. 1995

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Cyclosporine (CsA)-treated female Wistar rats, in dose of 37.5 μM (45 mg)/ kg/day for 7 days, exhibited significantly decreased creatinine clearance (Ccr), and provoked body weight loss (BWL), which is consistent with the development of nephrotoxicity (NT). Urine volume (V) did not change and proteinuria (PU) was not provoked. These changes were associated with significantly diminished ratios of urinary PGE₂/TXB₂ and 6kPGF_1α/TXB₂ excretions. Light-microscopic (LM) sections of rat kidneys showed that all kidneys were affected but the lesions (mainly diffuse vacuolization) were reversible. When CsA-treated animals were pretreated with ketanserine (KTS), which antagonizes (a) the direct vasoconstrictor effect of serotonin (5-HT), and (b) the amplifying effects of 5-HT on other vasoactive substances (such as noradrenaline (NA), α₁-receptors, histamine, H₂ receptors, and prostaglandin F_2α), Ccr and urine volume significantly increased, BWL was partially prevented and the ratios of urinary PGE₂/TXB₂ and 6kPGF_1α/TXB₂ excretions were significantly enhanced. LM sections showed that only 5 of 9 rats were affected but the lesions were of less importance. These observations indicate that the NT induced by CsA in our studies was mediated by 5-HT, a potent vasoconstrictor agent, and by the metabolites of arachidonic acid. However, other vasoactive agents and additional mechanisms could also be implicated.