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PubMed1989

Graft-versus-host resistance induced by tolerant cell populations. Evidence against clonal deletion as a mechanism of transplantation tolerance.

Characterization of the effect of immunization of F1 hybrid hosts with low doses of parental cells has shown that the F1 hybrid response to the receptor for the unshared MHC antigen on the immunizing cell induces specific resistance to a GVH challenge from cells of the same parental strain. We have shown that cells from parental rats tolerant to the unshared MHC antigens are capable of inducing GVH resistance in F1 hybrids. Unlike cells from normal parental rats that induce GVH resistance only when given in low immunizing doses of 10(6) cells, 10(6)-10(8) cells from tolerant donors effectively immunize F1 hybrids. This effect does not appear to be the result of passive transfer of suppressor cells from the tolerant donor. An alternative explanation is that tolerant populations contain cells that express the receptor for the tolerated alloantigen. The finding that normal parental populations that have been deleted of receptor-bearing cells by passage through semiallogeneic intermediate hosts do not induce GVH resistance, whereas tolerant cell populations do, confirms that clonal deletion does not adequately account for the functional characteristics of the tolerant cells. Attempts to delete putative receptor-bearing cells from the tolerant population however produced equivocal results.

Animals↗
PubMed1995

Detection of donor-derived cells by polymerase chain reaction in neonatally tolerant mice. Microchimerism fails to predict tolerance.

Although it has long been appreciated that establishment of chimerism is important in the acquisition and maintenance of allograft tolerance, the importance of this relationship has been reemphasized recently. Using the exquisite sensitivity of the polymerase chain reaction we have studied qualitatively and quantitatively the presence of donor-derived chimeric cells in relation to the ability of neonatally injected mice to display skin graft tolerance or rejection. We have found that virtually all mice that receive neonatal injections of F1 hematopoietic cells acquire donor-derived chimerism that is detectable in blood, spleen, lymph nodes, and thymus. Surprisingly, neither the presence nor the quantity of chimeric cells predicts whether a particular neonatally injected mouse will accept or reject donor-specific skin allografts. Moreover, whether the test skin allograft is accepted (tolerance) or rejected by neonatally injected mice, chimerism typically remains detectable within recipient lymphoid tissues. In functionally tolerant mice, challenge with a test skin allograft actually leads to a remarkable expansion in donor-derived genetic sequences, implying that donor-derived cells have been induced by the graft to undergo proliferation. Since persistence of chimerism without proliferation after test grafting is characteristic of mice that fail to display tolerance, we believe that achievement of a threshold level of donor-derived alloantigen may be necessary to retain the tolerant state. We conclude that chimerism is essential for the induction of neonatally induced tolerance, and its expansion may play an important role in the maintenance of that tolerance, when challenged by an allograft.

Animals↗
PubMed2004

Role of the thymus in transplantation tolerance in miniature Swine: IV. The thymus is required during the induction phase, but not the maintenance phase, of renal allograft tolerance.

BACKGROUND: The authors' laboratory previously demonstrated that long-term tolerance to class I-disparate renal allografts in miniature swine can be induced by a short course of cyclosporine A (CsA), and that this stable tolerance is dependent on the presence of an intact thymus. In the present study, the authors have examined the requirement for a thymus during the pretransplant, induction, and maintenance phases of tolerance. METHODS: Twenty-two miniature swine underwent class I major histocompatibility complex-mismatched renal transplantation, with a 12-day course of CsA. Thymectomies were performed on days -21, 0, +8, +21, and greater than or equal to +42, in relation to the day of transplantation. Historical controls consisted of euthymic and sham-thymectomized recipients. RESULTS: Euthymic, sham-thymectomized, and day-greater than or equal to +42 thymectomized recipients demonstrated stable renal function and minimal anti-donor cytotoxic T-lymphocyte (CTL) responses. In contrast, day -21 and day 0 thymectomized recipients demonstrated allograft dysfunction, marked cellular infiltrates, with severe vasculitis and glomerular changes, and strong anti-donor CTL responses. Animals thymectomized on days +8 and +21 did not undergo severe rejection, but likewise did not demonstrate a stable clinical course. CONCLUSIONS: These data indicate that the requirement for thymic function in the induction of rapid and stable tolerance is greatest during the first 8 days and then diminishes over the next 2 weeks posttransplant. Failure of thymectomy to affect the course of tolerance after day +21 suggests that thymic function is not required for the maintenance of tolerance. Understanding the role of the thymus in establishing tolerance may permit the development of tolerance induction strategies, especially for pediatric transplant recipients.

Animals↗
PubMed1983

Development of tolerance and cross-tolerance to the psychomotor actions of lorazepam and diazepam in man.

1 Development of tolerance and cross-tolerance to lorazepam and diazepam in man was assessed in a double-blind and cross-over trial where eight pretrained healthy students volunteered for four 1 week treatment periods started at 1 month intervals. 2 In each period acute psychomotor responses to oral lorazepam 3 mg and diazepam 15 mg were recorded on day 1, as well as on day 8 after 1 week's treatment twice daily with diazepam 5 mg, lorazepam 1 mg, and placebo. At each session several objective psychomotor tests and subjective assessments were done before the drug intake and 1, 2.5, and 4 h after it. 3 In general, the effects of lorazepam were stronger and of longer duration than those of diazepam at the doses used. When comparing the single-dose responses on days 1 and 8, tolerance to lorazepam effects and some cross-tolerance developed on several functions measured. Tolerance but not cross-tolerance developed on choice reaction errors whereas the opposite was found on flicker fusion. No definite tolerance was found on subjective effects. 4 The results tally with an assumption that tolerance to benzodiazepine actions develops at different rates on various parameters measured.

Adult↗
PubMed1986

Metabolic and functional aspects of tolerance to chlormethiazole and cross-tolerance to ethanol in the rat.

Adult male rats were used to study tolerance to, and physical dependence on, chlormethiazole and cross-tolerance to ethanol. In sleeping time studies, chlormethiazole was given orally at a daily dose rising progressively from 100 to 175 mg/kg over a period of 1 month. The tolerance that developed appeared to be due to altered disposition of the drug rather than to decreased sensitivity of the CNS. In agreement with this conclusion, there was only minimal cross-tolerance to ethanol, and no detectable withdrawal reaction. In studies with the moving belt test, the rats were given chlormethiazole subcutaneously in a total dose of 200 mg/kg daily for 69 days. This resulted in an equivocal manifestation of tolerance on the moving belt test and a small, but significant, tolerance to the hypothermic effect of chlormethiazole. Only an equivocal manifestation of physical dependence was found. These findings suggest that tolerance to the hypnotic and hypothermic effects observed with these chlormethiazole treatment regimens was due to altered pharmacokinetics rather than to functional tolerance of the CNS.

Animals↗
PubMed1992

Influence of ovarian steroids on myometrial sensitivity and tolerance to relaxin in the rat in vivo: lack of cross-tolerance between relaxin, salbutamol and cromakalim.

The influence of oestradiol benzoate and progesterone on uterine sensitivity and development of tolerance to relaxin was investigated in bilaterally ovariectomized non-pregnant rats in vivo. Bolus doses of relaxin (2-20 micrograms/kg i.v.) produced rapid and reversible inhibition of uterine contractions in a dose-dependent manner. Treatment with oestradiol benzoate or oestradiol benzoate plus progesterone significantly increased uterine sensitivity to relaxin over 48 h by 2.4- to 8.5-fold. Tolerance to relaxin developed during continuous infusion of the hormone at 20 micrograms/kg per h for 40 h. A 7.8- to 17.4-fold reduction in sensitivity to relaxin was observed in relaxin-infused rats, whereas no change in sensitivity was observed in saline-infused rats. Infusion of relaxin at 50 micrograms/kg per h for 40 h produced a 131.8-fold reduction in uterine sensitivity to relaxin. The uterus remained tolerant to relaxin for up to 24 h after cessation of infusion. Treatment with oestradiol benzoate and/or progesterone did not influence the extent of tolerance development, but a more rapid recovery of uterine sensitivity to relaxin was observed in rats treated with oestradiol benzoate plus progesterone. Cross-tolerance with other uterine relaxant drugs was measured to investigate possible common mechanisms of action and sites of tolerance between relaxin and a beta-adrenoceptor agonist (salbutamol) and potassium channel openers (cromakalim and minoxidil sulphate). No cross-tolerance was observed between relaxin and salbutamol, or relaxin and cromakalim or minoxidil sulphate. Cross-tolerance between cromakalim and minoxidil sulphate was seen.

Albuterol↗
PubMed1999

Transplantation tolerance: a look at the nonhuman primate literature in the light of modern tolerance theories.

Ever since the beginning of clinical transplantation, investigators have searched for a way to transplant tissues from one person to another without chronic immunosuppression. That goal, known as allograft tolerance, has remained clinically elusive. In the past decade, however, many of the fundamental principles of tolerance have been redefined, and biological agents capable of exploiting them in vivo have been developed. Accordingly, experimental methods for tolerance induction have rapidly evolved in concert with a growing understanding of physiological tolerance to self and the development of novel immunoreactive reagents. In general, old world monkeys have become the pre-clinical testing ground for methods that have shown reasonable promise for clinical application, particularly antibodies or other biological agents with limited cross-species reactivity. As such, a survey of the nonhuman primate experience in transplantation is representative of all reasonably successful experimental attempts to develop clinically applicable tolerance regimens. This article summarizes many of the concepts currently unfolding in the tolerance literature. It also reviews the techniques for tolerance induction that have been and are currently being investigated in nonhuman primates. The validity of these models is summarized, and the older literature is reinterpreted in light of recent changes in our understanding of tolerance.

ABO Blood-Group System↗
PubMed1976

The induction of hapten-specific T cell tolerance by using hapten-modified lymphoid cells. I. Characteristics of tolerance induction.

BALB/c mice were made tolerant to the T cell-dependent phenomenon of contact sensitivity to DNFB by i.v. injection of syngeneic lymphoid cells which had been previously modified with DNFB in vitro. The highly efficient unresponsiveness, as measured by ear challenge and in vitro antigen-induced cell proliferation, was shown to follow dose-response kinetics both in vivo and in vitro and to be exquisitely specific for the DNP moiety. The kinetics of tolerance induction were shown to be very rapid and had been previously shown to be long lasting. Unresponsiveness was more efficient when the hapten-modified cells were introduced by the i.v. route and tolerance could be increased by repeated injection of tolerogen. The tolerance could be transferred to normal syngeneic recipients by spleen and/or lymph node cells from tolerant donors. A wide variety of hapten-modified lymphoid cells, including mixed cell populations and enriched populations of T cells, B cells, and macrophages, were capable of inducing tolerance. The unresponsiveness was dependent merely on the association of DNP to the lymphoid membrane proteins and not upon the viability of the hapten-modified cells. These experiments support the hypothesis that in hapten-specific T cell sensitivity, as exemplified by contact sensitivity to DNFB, specific T cell tolerance in actively induced by hapten on self-membrane. In other hapten-specific antibody-forming systems, tolerance appears to be most readily induced by hapten on soluble self protein or on a nonimmunogeneic carrier.

Animals↗
PubMed1992

Tolerance to the cataleptic effect of the N-methyl-D-aspartate (NMDA) receptor antagonists in pigeons: cross-tolerance between PCP-like compounds and competitive NMDA antagonists.

The effects of chronic administration of phencyclidine (PCP) or CGS 19755 (cis-4-phosphonomethyl-2-piperidine-carboxylic acid) on the cataleptic effects of N-methyl-D-aspartate (NMDA) receptor antagonists were studied in pigeons. PCP, a channel blocker of the NMDA receptor complex, or CGS 19755, a competitive NMDA antagonist, was administered i.m. to separate groups of pigeons each day. Tolerance developed to the cataleptic effects in both PCP- and CGS 19755-treated pigeons. PCP tolerance was characterized initially by 5-fold rightward shift and, with an increased chronic PCP dose, a complete downward shift of the PCP dose-effect curve. CGS 19755 tolerance was indicated by a 10-fold rightward shift of its dose-cataleptic effect curve. Cross-tolerance was obtained from PCP to other PCP-like compounds including dizocilpine (MK 801), ketamine, dextrorphan, 1-(2-thienyl)-cyclohexyl-piperidine and [(+)-SKF 10047] [(+)-N-allyl-normetazocine] as well as to the competitive NMDA antagonist, CGS 19755. Cross-tolerance also developed from CGS 19755 to another competitive NMDA antagonist, CGP 40116 [D-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid] as well as to PCP-like compounds. The pharmacological selectivity of tolerance was evident because there was equal sensitivity to etomidate or pentobarbital in tolerant and nontolerant pigeons. The symmetric cross-tolerance between PCP-like compounds and competitive NMDA antagonists suggests the cataleptic effects of the two classes of NMDA antagonists are probably mediated via a similar mechanism of inhibition of neurotransmission at the NMDA excitatory synapse.

Animals↗
PubMed1984

Cholera toxin feeding did not induce oral tolerance in mice and abrogated oral tolerance to an unrelated protein antigen.

The feeding of protein antigens to mice results in a state of tolerance when feeding is followed by parenteral immunization. Cholera toxin (CT) is a protein that has been used extensively as a potent oral immunogen for mucosal IgA responses, but CT feeding also stimulates a substantial plasma IgG antibody response. This latter finding prompted us to study whether or not CT induces oral tolerance. Mice were fed 5 mg keyhole limpet hemocyanin (KLH) or 10 micrograms CT at least twice before parenteral immunization with 1 microgram KLH or CT in alum i.p. Plasma and intestinal secretions were collected at intervals. The specific IgG or IgA antibody in the samples was measured by ELISA. Although KLH feeding did induce oral tolerance, CT feeding did not induce oral tolerance in any of three mouse strains tested or at any dose of CT given orally. The feeding of the B subunit of CT did not result in oral tolerance either. When both CT and KLH were fed together, CT was able to abrogate oral tolerance to KLH, an antigenically unrelated protein. Moreover, feeding CT along with KLH stimulated secretory IgA anti-KLH responses, whereas no such IgA responses were found when KLH was given alone. Thus, in these experiments with protein antigens, IgA immunization and oral tolerance were reciprocally linked and did not occur simultaneously. CT appears to abrogate oral tolerance and to stimulate secretory IgA responses by altering the regulatory environment in gut-associated lymphoid tissue, shifting it toward responsiveness.

Administration, Oral↗
PubMed1982

Opiates and thermoregulation in mice. IV. Tolerance and cross-tolerance.

We have previously shown in mice that opiate agonists produce either hypothermia or hyperthermia or both, depending on the dose used and the ambient temperature. We have also shown that both temperature effects are blocked by the antagonists, naloxone and naltrexone. In order to confirm that these are specific opiate effects, the present studies to explore the development of tolerance to both temperature effects were undertaken. Mice were treated chronically with twice-daily injections of 2.5, 10, 40 or 160 mg/kg of morphine sulfate. Rectal temperature changes were monitored at 20 degrees, 25 degrees or 30 degrees C ambient temperature after the initial injection and at weekly intervals thereafter. At 20 degrees and 25 degrees C, the initial hypothermic response was replaced by hyperthermia after 7 weeks of twice-daily injections. At 30 degrees C, the initial hyperthermia became more pronounced and no evidence of tolerance was seen at any dose. A challenge dose of 160 mg/kg was given to all animals at 20 degrees C ambient temperature after 9 weeks of injections. There was a diminution of the hypothermic response inversely related to the chronically administered dose. At 30 degrees C, the 160 mg/kg challenge dose at 9 weeks showed little evidence of tolerance to the hyperthermia. Morphine-base pellet implantation, however, resulted in profound tolerance to both the hypo- and hyperthermic response within 1 day after implantation, peaking at 4 days and somewhat reduced by 1 week. Tolerance to the hypothermic effects induced by chronic administration of levorphanol and morphine-levorphanol cross-tolerance was also observed. It appears that both the hypo- and hyperthermia induced by the opiate and opioid agonists are opiate receptor effects because both effects can be blocked by the opiate antagonists and tolerance and cross-tolerance can be developed to both effects as well.

Animals↗
PubMed1978

Hapten-specific tolerance induced by hapten conjugates of D-glutamic acid, D-lysine (D-Gl) or isologous gamma-globulin: evidence for central B cell tolerance in the presence of carrier-primed helper T cells.

A comparison has been made of the well known hapten-specific tolerance systems induced, respectively, by hapten-D-GL or hapten-isologous gamma-globulin conjugates. The principal question addressed in this study concerned the comparative maintenance of B cell tolerance, induced by one or the other method, after adoptive transfer into carrier-primed, irradiated recipient animals and, in addition, what role, if any, might be played by T lymphocytes in the tolerant donor cell population in maintaining such tolerance. The results clearly show that insofar as the hapten-specific B cell is concerned, no obvious difference exists in the capacity to maintain tolerance adoptive transfer between the hapten-D-GL and hapten-isologous gamma-globulin systems; such cells remained tolerant even in the presence of excess helper T cell activity. Moreover, under the conditions employed, depletion of T lymphocytes from the tolerant donor cell population did not affect the maintenance of hapten-specific B cell tolerance after adoptive transfer to irradiated recipients.

Animals↗
PubMed1993

Cocaine tolerance and cross-tolerance.

Pharmacological mechanisms by which tolerance develops to the behavioral effects of cocaine were assessed by examining cross-tolerance to specific drugs. Daily experimental sessions were conducted in which rats were trained to press a key under a fixed-ratio 30-response schedule of food reinforcement (each 30th response produced food). Each of the drugs studied decreased rates of responding before initiating daily (10 mg/kg, i.p.) treatment with cocaine. Treatment with cocaine produced a small, significant shift to the right in the cocaine dose-effect curve; the ED50 values changed from 13.3 to 21.7 mg/kg. Cross-tolerance was not conferred to the indirect agonist, d-amphetamine, the direct agonist apomorphine, the D1-selective agonists SKF 38393 or fenoldopam, or the D2-selective agonists quinpirole or (-)-NPA. Cross-tolerance was conferred to the close structural analog of cocaine, WIN 35,428, but not to another dopamine uptake inhibitor, GBR 12909. Tolerant rats showed no change in specific binding of [3H]SCH 23390 to D1 receptors, [3H]spiperone to D2 receptors, [3H]GBR 12935 to dopamine uptake sites in striatum, [3H]paroxetine to serotonin uptake sites or [3H]mazindol to norepinephrine uptake sites in cortex or hippocampus. In addition, there were no changes in transmitter levels indicative of neurotoxicity. Serum levels of cocaine were not appreciably different in groups of cocaine- and saline-treated rats. The present results suggest that the modest tolerance that can develop to the behavioral effects of cocaine does not confer significant functional or metabolic changes in the effects of drugs acting on dopaminergic systems. Importantly, the tolerance produced by repeated administration of cocaine does not produce a cross-tolerance to GBR 12909, suggesting differences in mechanism among different structural forms of dopamine uptake inhibitors.

Animals↗
PubMed1993

A comparison of the effects of chronic nicotine infusion on tolerance to nicotine and cross-tolerance to ethanol in long- and short-sleep mice.

Several recent studies suggest that common genes regulate sensitivity to an acute dose of ethanol and nicotine. The studies reported here attempted to determine whether common genes regulate the development of cross-tolerance between these drugs. Long-sleep (LS) and short-sleep (SS) mice, which were selectively bred for differential sensitivity to ethanol as measured by duration of ethanol-induced anesthesia (sleep time), were used in this study. The mice were infused i.v. with saline (control) or one of several doses of nicotine (0.5-4.0 mg kg-1 hr-1) for 10 days. The LS mice were more sensitive to the acute actions of nicotine than were the SS and they developed more tolerance to nicotine. LS mice were tolerant to nicotine as measured by all four of the behavioral and physiological tests used but this tolerance was readily seen only after treatment with the highest infusion dose. The SS mice developed some tolerance to nicotine but this effect was less than that seen in the LS, was restricted to two of the tests (Y-maze crosses and body temperature) and was seen only after treatment with the 4.0-mg kg-1 hr-1 dose of nicotine. The LS mice developed cross-tolerance to ethanol as measured by the Y-maze crosses and the heart rate and body temperature tests. Cross-tolerance to ethanol was not seen in the LS mice for the Y-maze rears and sleep-time tests. Almost no evidence for cross-tolerance to ethanol was seen in nicotine-infused SS mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Acquired thymic tolerance: role of CTLA4 in the initiation and maintenance of tolerance in a clinically relevant autoimmune disease model.

Injection of Ag into the thymus of adult animals induces specific systemic tolerance. The mechanisms of acquired thymic tolerance include anergy and the deletion of Ag-specific T cells. Here, we report that anergy to nominal Ag induced via acquired thymic tolerance requires CTL-associated Ag 4 (CTLA4) engagement. The role of CTLA4 in the induction and maintenance of tolerance was then investigated in the murine experimental autoimmune encephalomyelitis model. CTLA4 blockade abrogated the induction but not the maintenance phase of acquired thymic tolerance induced by intrathymic injection of myelin Ags. In addition, CTLA4 blockade had a restricted window of action after priming with Ag, which is consistent with the expression patterns of CTLA4 in vivo. We conclude that: 1) the induction of acquired thymic tolerance requires signaling through CTLA4 and 2) CTLA4 does not appear to be required for the maintenance of acquired thymic tolerance. This is the first report documenting the role of a CTLA4 negative signaling pathway in the induction of tolerance in an autoimmune disease model.

Abatacept↗
PubMed2005

Study of calcium-dependent lead-tolerance on plants differing in their level of Ca-deficiency tolerance.

The main aim of the study was to determine the role of calcium in the amelioration of lead toxic effects in plants with accordingly high/low level of Pb-tolerance and high/low Ca-deficiency tolerance. The study was performed on maize, rye, tomato and mustard. Plants were cultivated in modified Knop's solution. They were subjected to Ca-deficiency, and to lead nitrate administered in the presence of four calcium nitrate concentrations 3.0, 2.4, 1.2, 0.3mM. Lead-tolerance and tolerance to Ca-deficiency were determined, as were concentration of the studied elements in plant tissues, and the Pb deposition pattern at the ultrastructural level (electron microscopy study, X-ray microanalysis). In all studied plants, lead toxicity increased as medium calcium content decreased, however, only in the Ca-deficiency sensitive mustard with low Pb-tolerance was it accompanied by a rise in tissue lead concentration. In contrast, lead root and shoot levels did not increase in the highly Ca-deficiency tolerant tomato, mustard and rye with high Pb-tolerance irrespective of the Ca(2+) regimens applied. Thus, in these plants, lead's unfavourable effects resulted only from the higher toxicity of the same amount of lead in tissues at low calcium in the medium. Of particular relevance is the finding by electron microscopy and X-ray microanalysis, that under low calcium in both highly Ca-deficiency tolerant and Ca-deficiency sensitive plants, less efficient Pb(2+) detoxification was accompanied by the restriction of the formation of large lead deposits in cell walls. Obtained results are novel in demonstrating calcium involvement in the lead deposition in the cell wall, thus in the regulation of the internal lead detoxification.

Air Pollutants↗
PubMed2004

Improvements in glucose tolerance in obese males with abnormal glucose tolerance following 10 days of aerobic exercise.

BACKGROUND: Aerobic exercise training has been shown to produce beneficial changes in glucose tolerance and insulin sensitivity in obese individuals if performed at high enough intensities and/or durations. We examined the effects of a moderate intensity, short-term exercise training protocol on glucose tolerance in obese males with glucose intolerance. METHODS: Fourteen abdominally obese, sedentary males with normal glucose tolerance (NGT; n = 7) and abnormal glucose tolerance (AGT; n = 7) completed 40 min of exercise bouts for 10 consecutive days at approximately 75% of age-predicted maximum heart rate. Fasting glucose and insulin levels, and glucose tolerance and insulin response to glucose were measured before and after the training period. RESULTS: Participants did not experience significant mass loss during the 10-day investigation. Individuals in the AGT group experienced significant (P < 0.05) improvement in glucose tolerance [glucose area: 1,763.67 (255.98) mmol L(-1) x 120 min(-1) vs. 1,682.98 (266.91) mmol L(-1) x 120 min(-1)] and fasting insulin levels [44.57 (7.58) microU mL(-1) vs. 36.14 (3.97) microU mL(-1)] as a result of training. Significant (P < 0.05) reductions in fasting glucose concentrations [5.82 (0.19) mmol L(-1) vs. 5.42 (0.18) mmol L(-1)] and a decrease in fasting insulin concentrations [44.71 (9.39) microU mL(-1) vs. 35.0 (7.15) microU mL(-1); P = 0.064] were observed in the NGT group following the training period. CONCLUSIONS: The data suggest that moderate, short-term exercise without concomitant mass loss is effective in improving glucose tolerance and insulin response to a glucose load in obese males with abnormal glucose tolerance.

Adult↗
PubMed1994

Efficacy of ciprofloxacin in treatment and prophylaxis of experimental Staphylococcus aureus endocarditis caused by a cloxacillin-tolerant strain and its non-tolerant variant.

The efficacy of ciprofloxacin in treatment and prophylaxis of Staphylococcus aureus endocarditis in rats infected with a strain tolerant to the standard anti-staphylococcal antibiotics cloxacillin, vancomycin and teicoplanin was compared with its non-tolerant variant. After 5 days of treatment with ciprofloxacin 30 mg/kg subcutaneously every 8 h bacterial densities in vegetations from animals infected with the tolerant and the non-tolerant strain were similar. Resistance to ciprofloxacin did not emerge in either strain of S. aureus during treatment. In prophylaxis experiments a single dose of ciprofloxacin (30 mg/kg) administered 30 min before bacterial challenge afforded almost full protection for both the tolerant and the non-tolerant strain. At a lower dose of 6 mg/kg the protective effect was less compared with the higher dose, but no difference in the proportion of sterile vegetations was found between the two strains. Thus tolerance influenced neither treatment nor prophylaxis with ciprofloxacin. For strains of S. aureus tolerant to the usual anti-staphylococcal antibiotics ciprofloxacin could be a useful alternative for the treatment of infections.

Animals↗