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Biomedical subjects

B Rouveix

Publications and source records attributed to B Rouveix.

At least 37 records · Page 2Linked to original sources
PubMed1991

Immune status and survival of opiate- and cocaine-treated mice infected with Friend virus.

In as much as the immunomodulatory effects of opiates and cocaine are known to modify spontaneous host defenses against infection, we investigated the effects of morphine, pentazocine and cocaine on the time course of Friend virus infection in mice. Repeated i.p. injections with increasing doses of morphine hydrochloride (10-100 mg/kg for 10 days before infection, a dose regimen which induced tolerance to the acute antinociceptive effects of the drug, followed by 30 mg/kg for 14 days postinfection) did not increase the mortality due to Friend virus infection. This regimen did not significantly affect the immune response of infected mice assessed in terms of delayed hypersensitivity (ear thickness) and the hemagglutination assay. In contrast, a single challenge with a large dose of morphine (up to 300 mg/kg), which is not lethal in noninfected mice, increased mortality markedly (up to 100%) in infected mice when administered at day 14 or 21 postinfection. Repeated i.p. injections with pentazocine (50 mg/kg b.i.d. for 5 days before infection, followed by 30 mg/kg for 14 days postinfection) had no influence on mortality or immune responses in infected mice; similar results were obtained with a single high-dose injection (up to 100 mg/kg). Lastly, repeated i.p. injections of cocaine, using the same experimental procedure as that for pentazocine, decreased immune responsiveness and slightly increased mortality, whereas a single injection was devoid of lethal effect. These findings suggest that chronic opioid treatment does not lower host resistance to viral infection but that the latter could increase the toxicity of a single high dose of morphine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1990

T activation marker evaluation in ARC patients treated with AZT. Comparison with CD4+ lymphocyte count in non-progressors and progressors towards AIDS.

Reductions in the percentage and absolute number of CD4+ lymphocytes, as well as abnormally high levels of activated peripheral T lymphocytes (CD3+ HLA-DR+ phenotype) and an increased proportion of CD8+ cells coexpressing the CD57 surface antigen (involved in natural killer activity) have been reported in HIV infection and associated with disease progression. We prospectively measured these subsets of lymphocytes in 34 patients with advanced AIDS-related complex (ARC) treated with azidothymidine (AZT). Peripheral blood lymphocyte phenotyping was performed before treatment, then at weeks 12 and 24. A striking fall in the proportion of activated T lymphocytes from baseline was observed (P less than 0.001) at week 24. In contrast, the percentage of CD4+ cells showed a slight and transient rise at week 12 (P less than 0.05). No modification in levels of CD8+ or CD8+ CD57+ cells was detected during the study. Of the 34 patients, 11 developed AIDS, and 23 remained AIDS-free during 51 weeks of follow-up. Similar patterns of change in CD4+ and HLA-DR+ CD3+ lymphocytes were found in the AIDS progressors and nonprogressors. Likewise, HIV p24 antigenaemia showed parallel decreases in both groups of patients. Although changes in CD4+ cells, p24 antigenaemia and HLA-DR-reactive T lymphocytes were not predictive of clinical outcome, large differences existed between the two groups prior to the initiation of therapy. The short-term onset of AIDS was associated with lower CD4+ cell numbers, higher levels of serum p24 antigen and a greater proportion of activated T lymphocytes. Our results suggest that the possible interest of T lymphocyte activation markers, in conjunction with conventional phenotyping, should be investigated further.

AIDS-Related Complex↗
PubMed1990

In vivo assessment of antimicrobial agents against Toxoplasma gondii by quantification of parasites in the blood, lungs, and brain of infected mice.

The in vivo effects of antimicrobial agents against Toxoplasma gondii were evaluated in mice that were infected intraperitoneally with 10(4) tachyzoites of the RH strain by determination of survival rates and study of the kinetics of growth of T. gondii in infected mice. At various intervals after infection, subcultures of serial dilutions of blood, lung, and brain homogenates were performed in fibroblast tissue cultures for determination of parasitic loads. Pyrimethamine (18.5 mg/kg per day), sulfadiazine (375 mg/kg per day), and clindamycin (300 mg/kg per day) were administered for 10 days from day 1 or day 4 after infection. Untreated control mice died within 9 days and showed early and predominant lung involvement. All mice treated with sulfadiazine administered from day 1 survived and were apparently healthy; parasitic loads decreased early after treatment, but a relapse was observed 5 days after the cessation of therapy. When pyrimethamine was administered from day 1, 7 of 11 mice died within 25 days; by determination of parasitic loads, the effect of pyrimethamine was only demonstrable from day 6, and a relapse was constantly observed after the cessation of therapy. When pyrimethamine and sulfadiazine were administered in combination, 100% of mice survived; when therapy was started at day 1, parasites remained undetectable; in mice treated from day 4, parasites were eradicated by day 8 but infection relapsed 8 days after the cessation of therapy. All mice treated with clindamycin from day 1 or day 4 died within 10 days, but parasitemia was always undetectable. These results indicate that study of the kinetics of parasitic loads in blood and organs may provide additional information on the effect of antimicrobial agents against T. gondii in regard to the evolution of the infection and may represent a reliable basis for the determination of therapeutic regimens in humans.

Animals↗
PubMed1990

[Good tolerance and absence of immunologic effects in mice treated with arsenic-rich thermal water].

Three strains of mice were given, per os and ad libitum, a spa water containing 6.8 mg/l arsenic and indicated for the treatment of allergic respiratory diseases or chronic bronchitis. The daily arsenic intake was approximately from 1.5 to 4 mg/kg. No effect on body weight gain or on the various immune parameters assessed was observed. These results demonstrate that this spa water, despite its high arsenic content, is not toxic and does not interfere with the immune system of healthy mice.

Animals↗
PubMed1989

Effect of zinc on the immune status of zinc-depleted AIDS related complex patients.

Zinc deficiency has been recently reported in AIDS patients to be associated with a decrease in T helper cells. The effect of zinc supplementation was evaluated in 5 ARC patients and 5 control subjects using lymphocyte subset counts, blast transformation and chemiluminescence of polymorphonuclear leukocytes. Zinc was analysed by atomic absorption spectrophotometry. T-cell subsets were quantified by cytofluorometry. Chemiluminescence of PMN was measured by phagocytosis of opsonized zymosan. The ARC patients had significantly lower zinc concentrations in the RBC prior to supplementation (p < 0.05). This level increased following the administration of zinc gluconate. This increase was accompanied by (i) an increase in HLA.Dr + cells with no CD4 CD8 ratio alteration; (ii) a stimulation of lymphocyte transformation and PMN chemiluminescence particularly after 15 days' high zinc supplementation. Such a reconstitution in specific and non specific immune functions in ARC patients may warrant further investigation.

Journal Article↗
PubMed1989

Divided-dose kinetics of mefloquine in man.

The kinetics of mefloquine was investigated following oral divided-doses in 10 healthy Caucasian volunteers. They received 500 or 750 mg followed by 500 mg 8 h later. Unchanged mefloquine (M) and its carboxylic acid metabolite (MM) were measured in whole blood and plasma for 50 days by h.p.l.c. Maximum blood and plasma M concentrations of 1872 +/- 362 ng ml-1 (mean +/- s.d.) and 1900 +/- 434 ng ml-1, respectively, were found within 6-10 h after the second dose. The terminal plasma elimination half-life was 20.1 +/- 3.7 days (mean +/- s.d.) and the oral clearance was 22.3 +/- 6.7 ml h-1 kg-1 (mean +/- s.d.). Plasma concentrations of MM exceeded those of M by 2-3 fold within 2 days. The whole blood concentration of MM was lower than that in plasma but also exceeded the whole blood concentration of M.

Adult↗
PubMed1989

Amodiaquine-induced immune agranulocytosis.

This report describes two patients who developed agranulocytosis while receiving prophylactic amodiaquine treatment. The neutrophil counts returned to normal in one after stopping the drug while the other died of sepsis. Amodiaquine-dependent circulating neutrophil IgG antibodies were demonstrated in both patients using the indirect granulocyte immunofluorescence test. The antineutrophil antibody activity was enhanced with the use of the major amodiaquine metabolite, mono-desethyl amodiaquine. Additional studies showed the activity of the sera to be nondialysable, heat stable, active against autologous as well as allogenic cells, and absent from the convalescent sera. There was no growth inhibition of allogenic myeloid committed progenitor cells (CFU-GM) following incubation with the patients' sera, complement and amodiaquine. These results indicate that agranulocytosis can be mediated by a drug-dependent antibody which affects mature blood cells.

Agranulocytosis↗
PubMed1989

Amodiaquine-induced agranulocytosis: report of a case with in vitro studies of granulocyte-macrophage progenitor cells.

We report a case of amodiaquine-induced agranulocytosis in a 60-year-old woman. Four months after the agranulocytosis episode we investigated the effect of the drug using in vitro agar culture techniques. Amodiaquine at increasing concentrations (0.005, 0.05 and 0.5 microgram/ml) displayed an inhibitory effect, probably dose-dependent, on the growth of the patient's bone marrow GM-CFU colonies in the absence of autologous serum. In contrast, no effect was found on the colony and cluster growth of bone marrow samples from 13 healthy controls. Though it has been shown in several cases that amodiaquine-induced agranulocytosis occurs via immune-mediated mechanisms, our data are in support of a direct toxic effect of the drug on abnormally sensitive myeloid progenitor cells.

Agranulocytosis↗
PubMed1987

Beta-lactam antibiotics and human lymphocyte function: the in vitro effect on blastogenesis, lymphokine production and suppressor cell functions.

The effects of penicillin, cephalothin and cefoxitin on lymphokine production and mitogen stimulation of human peripheral blood lymphocytes and suppressor cell functions in man were studied with concentrations achievable in serum. Penicillin (50 and 100 micrograms/ml) and cephalosporins (50 and 100 micrograms/ml) directly stimulated production of the lymphokine leukocyte aggregating factor (LAgF) by unstimulated lymphocytes and enhanced mitogen-stimulated production of this lymphokine. Neither beta-lactam derivative interfered directly with neutrophil aggregation. Using the same concentration, penicillin did not suppress but had either no effect on or slightly increased the unstimulated and mitogen-stimulated lymphocyte transformation responses, whereas cephalosporins significantly suppressed both responses. Suppression of blastogenesis by the latter could be mediated through suppressor cell enhancement as indicated by the significant suppressed lymphocyte transformation observed while using the supernatant of cephalosporin-stimulated and cultured lymphocytes. This suppressive activity was more pronounced with cephalothin than with cefoxitin while it was not observed with penicillin which rather stimulated thymidine uptake. These findings suggest that enhancement of lymphokine production and suppression of lymphocyte transformation by cephalosporins are not contradictory and reflect a stimulating effect on two different lymphocyte subsets. The enhancement of suppressor function might account for the lower incidence of late hypersensitivity reactions observed in patients treated with the cephalosporins compared with those treated with penicillins.

Cefoxitin↗
PubMed1987

[Action of cephalosporins on T lymphocytes: the role of mediators].

The in vitro effect of various cephalosporins on T lymphocyte functions was studied. These antibiotics directly stimulated lymphokine production and significantly suppressed mitogen-stimulated lymphocyte transformation responses. Penicillin had no effect. Suppression of blastogenesis could be mediated through suppressor cell enhancement as indicated by: i) the significant suppressed lymphocyte transformation observed while using the dialyzed supernatant of cephalosporin-stimulated and cultured lymphocytes, ii) the enhanced blastogenesis, commonly ascribed to suppressor cell depletion, blunted by pre-incubation with cephalosporins, iii) the suppressed blastogenesis of allogenic responder cells in MLR by cephalosporin pre-incubated, mitomycin treated cells. An indirect effect through PgE2 release by macrophages cannot ruled out. The enhancement of suppressor activity by most of the cephalosporins might explain the smaller incidence of late hypersensitivity reactions observed with these antibiotics compared with penicillins.

Adult↗
PubMed1986

Activated human lymphocytes secrete a soluble factor that aggregates leukocytes.

Human polymorphonuclear leukocytes can be activated by various inflammatory stimuli to display increased cell aggregation which is potentially an important pathogenetic mechanism. This study describes a soluble factor produced by concanavalian A-stimulated lymphocytes that causes human leukocytes to aggregate. This factor could be assayed quantitatively by measuring the light absorbance of polynuclear leukocyte suspension using a spectrophotometer. The lymphokine involved, namely the leukocyte aggregating factor (LAgF) was released by non pulse exposure to the mitogen for up to 72 hr with a maximum at 48 hr. LAgF was characterized by Sephadex gel filtration, chromatofocusing, enzymatic and chemical treatment. Sephadex G 100 gel filtration showed LAgF activity in a molecular range of 40,000-65,000. Chromatofocusing of culture supernatant showed LAgF in a single broad peak (4.8-5.4) with a maximum activity at pI 5.2. Human LAgF was heat sensitive, inactivated by treatment with chymotrypsin, and not affected by neuraminidase. Activity was partially recovered from the supernatant after protein precipitation with 1 M perchloric acid and not destroyed by 0.02 M sodium periodate. These findings characterize LAgF as a protein. These data suggest that LAgF is not different from leukocyte inhibiting factor by virtue of its size and physiological properties.

Cell Adhesion Molecules↗