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Results for “Roxithromycin”

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PubMed1999

Determination of roxithromycin in human plasma by high-performance liquid chromatography with spectrophotometric detection.

A simple and reproducible method for the determination of roxithromycin in human plasma is presented. This method is based on liquid-liquid extraction with hexane-isoamylalcohol (98:2, v:v) and reversed-phase chromatography with spectrophotometric detection at 220 nm. The mobile phase consists of methanol-15 mM dihydrogen potassium phosphate (70:30, v:v), pH of the aqueous part of the mobile phase is 6.0. The column is operated at 60 degrees C. Clarithromycin is used as the internal standard. The limit of quantitation is 0.5 microg/ml and the calibration curve is linear up to 30 microg/ml. Within-day and between-day precision expressed by relative standard deviation is less than 5% and inaccuracy does not exceed 9%. The assay was used for pharmacokinetic studies.

Anti-Bacterial Agents↗

PubMed1996

Effect of new macrolide roxithromycin upon nasal polyps associated with chronic sinusitis.

We often observe shrinkage of nasal polyps with low-dose long-term macrolide treatment, which was recently developed in Japan for the treatment of intractable chronic sinusitis. In order to assess the efficacy of this treatment for nasal polyps, we administered the new macrolide roxithromycin (RXM) (1 tablet: 150 mg a day) for at least 8 weeks to 20 patients with nasal polyps associated with chronic sinusitis. It was competent in controlling nasal polyp with the overall incidence of improvement being 52%. The combination of RXM with azelastine (1 mg twice/day), an inhibitor of mediator release, was examined in 20 other patients. It augmented the rate of improvement to 68%, but the increase was not significant. The incidence of improvement increased with time after the start of medication in both groups. Smaller polyps were more likely to decrease in size, but some larger polyps also markedly decreased in size. Associated allergic conditions and the extent of eosinophilic infiltration had no relation to the treatment result. We speculate that the mechanism of effectiveness of RXM is through its suppressive potency in cytokine production from inflammatory cells.

Adult↗

PubMed2001

Potential anti-androgenic activity of roxithromycin in skin.

Since acne formation is a multistep process accelerated by androgens, we examined whether a new anti-acne antibiotic roxithromycin (RXM) may act as anti-androgen using transient transfection assays in human skin fibroblasts. The result showed no significant effect of 0.5, 1 and 5 microg/ml RXM on 10(-9) M R1881-induced androgen receptor (AR) transcriptional activity. While the cotransfection of exogenous ARA55, a novel AR coactivator, increased AR transactivation up to 2.59-fold, this increase was attenuated by 5 microg/ml RXM to 64.7%. Semiquantitative RT-PCR results showed that 0.1 mM H(2)O(2) treatment increased ARA55 mRNA expression level, indicating that reactive oxygen species increase the expression of ARA55 in skin. These results suggest that RXM may serve as anti-androgen only in the hypersensitive state to androgen, but not in the physiological state, through modulating end-organ hypersensitive condition to androgen possibly involving the pathway from reactive oxygen species to ARA55.

Androgen Antagonists↗

PubMed1998

Roxithromycin down-modulates antigen-presenting and interleukin-1 beta-producing abilities of murine Langerhans cells.

The immunomodulatory effect of the macrolide antibiotic, roxithromycin (RXM) on Langerhans cells (LC) was studied in mice. RXM inhibited the ability of LC to present superantigen and hapten to T cells at 100 microM. The superantigen-presenting activity of LC was more profoundly abrogated by RXM than the hapten-presenting activity. This functional reduction was partly attributed to an RXM-induced decrease in promotion of the expression of major histocompatibility complex class II molecules on LC. On the other hand, RXM down-modulated the production of interleukin-1 beta by LC at a lower concentration of 10 microM than concentrations that inhibited antigen presentation. These results imply that RXM exerts therapeutic effectiveness via not only bacteriocidal action but also inhibitory effect on the LC ability in T-cell-mediated cutaneous diseases that can be exacerbated by skin-colonized Staphylococcus aureus.

Animals↗

PubMed2001

Effect of roxithromycin on T lymphocyte proliferation and cytokine production elicited by mite antigen.

Clinical evidence suggests that roxithromycin (RXM) may be an effective additional therapy for bronchial asthma. However, how it interferes with allergic responses is unclear. To investigate the mechanisms of action of RXM, lymphocyte transformation and interferon (IFN)-gamma, interleukin (IL)-4 and IL-5 synthesis associated with Dermatophagoides farinae (Df), mite antigen in patients with bronchial asthma were evaluated in vitro in the presence of RXM. T cell proliferation in Df antigen-stimulated patients' lymphocytes was suppressed by 50-100 microg/ml of RXM. Production of IL-4 and IL-5 was similarly decreased by 1-10 microg/ml RXM, whereas, IFN-gamma production, which was reduced by Df-stimulation alone, was increased by 50 microg/ml RXM. Our results suggest that skewed cytokine profiles of patients with mite antigen-induced bronchial asthma may be corrected with RXM, which may mimic those of patients in remission, who are tolerant of Df antigen.

Adolescent↗

PubMed2001

Suppression of co-stimulatory molecule expressions on splenic B lymphocytes by a macrolide antibiotic, roxithromycin in vitro.

The influence of a macrolide antibiotic, roxithromycin (RXM), on co-stimulatory molecule expression was examined using in vitro cell culture technique. Spleen cells obtained from BALB/c mice 10 days after immunization with 8.0 micrograms of haemocyanin absorbed to 4.0 mg aluminum hydroxide were cultured in the presence of 100.0 micrograms/ml haemocyanin and various concentrations of RXM for 72 h. Low concentrations (1.0 and 2.5 micrograms/ml) of RXM did not influence cell activation induced by antigenic stimulation, whereas RXM showed a suppressive effect on blastic activity of the cells when the agent was added to the cultures at more than 5.0 micrograms/ml. RXM did not affect blastic activity of splenic T cells by anti-CD3 monoclonal antibody stimulation even when the cells were cultured in the presence of 10.0 micrograms/ml RXM. Addition of anti-CD80 and anti-CD86 monoclonal antibody to cell cultures caused significant suppression of cell activation by antigenic stimulation. We next examined the influence of RXM on co-stimulatory molecule expressions on splenic B cells in response to antigenic stimulation. Addition of RXM at a concentration of 5.0 micrograms/ml into cell cultures remarkably suppressed co-stimulatory molecule, CD40, CD80 and CD86, expressions, which enhanced by antigenic stimulation in vitro.

Animals↗

PubMed2001

Modulation of Th2 type cytokine production from human peripheral blood leukocytes by a macrolide antibiotic, roxithromycin, in vitro.

The influence of a macrolide antibiotic, roxithromycin (RXM), on Th1 and Th2 cytokine productions from human peripheral blood T cells was examined under stimulation with co-stimulatory molecules. Peripheral blood T cells prepared from both healthy and allergic rhinitis donors were cultured in the presence of RXM on anti-CD3 mAb and anti-CD26 mAb-coated wells, anti-CD3 mAb and anti-CD28 mAb-coated wells, and anti-CD3 and PMA. T-cell proliferation, along with the concentration of interleukin (IL)-2, interferon (IFN)-gamma, IL-4 and IL-5 were measured. RXM did not affect T-cell proliferation induced by several ways of co-stimulatory activation as assessed by 3H-thymidine incorporation into DNA. RXM also had no effect on IL-2 and IFN-gamma secretion by T cells prepared from both healthy and allergic rhinitis donors. On the other hand, RXM markedly inhibited both IL-4 and IL-5 secretions under each of the co-stimulatory conditions in a dose-dependent manner. These results indicate that RXM inhibits specifically Th2 cytokine secretion from T cells induced by co-stimulatory molecule stimulations. This inhibitory action of RXM may be partially responsible for attenuating effect of the agent on the inflammatory diseases.

Adult↗

PubMed1997

Roxithromycin, clarithromycin, and azithromycin attenuate the injurious effects of bioactive phospholipids on human respiratory epithelium in vitro.

The effects of the bioactive phospholipids (PL), platelet-activating factor (PAF), lyso-PAF, and lysophosphatidylcholine (LPC) on the beat frequency and structural integrity of human ciliated respiratory epithelium were studied in vitro, in the presence or absence of polymorphonuclear leukocytes (PMNL), the antimicrobial agents, roxithromycin, clarithromycin, and azithromycin and the antioxidative enzymes catalase and superoxide dismutase (SOD). All three PL caused dose-dependent slowing of ciliary beat frequency (CBF) and epithelial damage (ED) at concentrations > or = 1 microgram/ml, which were unaffected by inclusion of the antimicrobial agents and antioxidative enzymes. When epithelial strips were exposed to the combination of PMNL and PL, there was significant potentiation of ciliary dysfunction and ED, which was ameliorated by pretreatment of the PMNL with the antimicrobial agents or by inclusion of catalase, but not SOD. These results demonstrate that LPC, PAF, and lyso-PAF cause epithelial damage by direct mechanisms which are oxidant-independent, as well as by indirect mechanisms involving phagocyte-derived reactive oxidants. Macrolides and azalide antimicrobial agents may have beneficial effects on airway inflammation in asthma and microbial infections by protecting ciliated epithelium against oxidative damage inflicted by PL-sensitized phagocytes.

Anti-Bacterial Agents↗

PubMed2003

Influence of roxithromycin on inflammatory cytokine production from nasal polyp fibroblasts in vitro.

The influence of macrolide antibiotics, roxithromycin (RXM) and josamycin (JM) on inflammatory cytokine production from human nasal polyp fibroblasts (NPFs) was examined using an in vitro cell culture technique. Addition of RXM at a concentration of 10.0 microg/ml to cell cultures suppressed both IL-6 and RANTES (but not IL-8) production in response to stimulation with 25.0 ng/ml tumor necrosis factor (TNF)-alpha. However, JM could not suppress IL-6, IL-8 and RANTES production from NPFs induced by TNF-alpha stimulation in vitro, even when added to cell cultures at a concentration of 20.0 microgram/ml. In the second part of the study, we examined the influence of RXM on cytokine mRNA expression in NPFs. Addition of RXM at a concentration of 10.0 mg/ml to cell cultures caused reduction of the mRNA expressions of both IL-6 and RANTES, which were enhanced by TNF-alpha stimulation in vitro.

Anti-Bacterial Agents↗

PubMed1998

Effect of roxithromycin on IL-8 synthesis and proliferation of nasal polyp fibroblasts.

Although several studies have demonstrated that low-dose, long-term 14-member macrolides (erythromycin (EM), roxithromycin (RXM), clarithromycin (CAM)) are effective in the treatment of chronic airway diseases like chronic sinusitis and diffuse panbronchiolitis (DPB), the mechanism of action of these drugs is not yet clear. Both these airway diseases are associated with an increase in the proliferation of fibroblasts. Moreover, fibroblasts are also an important source of proinflammatory cytokines such as interleukin-8 (IL-8), that play an important role in the pathogenesis of nasal polyps. Therefore, using primary fibroblast lines derived from nasal polyps, we investigated the effect of RXM on the synthesis of IL-8 and proliferation of nasal polyp fibroblasts (NPF). These fibroblasts were either treated with lipopolysaccharide (LPS) and RXM for 24 h, or pre-incubated with RXM for 24 h and then treated with LPS and RXM for 24 h. The level of IL-8 mRNA in NPF was analysed by reverse transcriptase-polymerase chain (RT-PCR) and the level of IL-8 in culture supernatants was measured by ELISA. Next, the proliferative capacity of NPF after treatment with RXM was analysed by cell counting and 3H-thymidine uptake. RXM had no effect on LPS-induced IL-8 synthesis by NPF. On the other hand, RXM suppressed the proliferation of NPF in a dose-dependent manner. These findings suggest that, although RXM cannot directly inhibit the synthesis of IL-8, it probably reduces IL-8 production by inhibiting the proliferation of NPF.

Anti-Bacterial Agents↗

PubMed2000

Suppressive activity of a macrolide antibiotic, roxithromycin on co-stimulatory molecule expression on mouse splenocytes in vivo.

The influence of roxithromycin (RXM) on the expression of co-stimulatory molecules, CD40, CD80 and CD86, was examined in vivo. When BALB/c mice were immunized intraperitoneally with two doses of dinitrophenylated ovalbumin (DNP-OVA) at 1 week intervals, intraperitoneal administration of RXM at 250 microg/kg once a day for 14 days strongly suppressed IgE contents in sera obtained from mice 22 days after the first immunization. In addition, RXM treatment of mice suppressed endogenous IL-4 contents in aqueous spleen extracts, which were enhanced by DNP-OVA immunization. We next examined the influence of RXM on co-stimulatory molecule expression on splenic lymphocytes. RXM treatment of the immunized mice caused suppression of CD40 expression, but this treatment did not affect CD80 and CD86 expression.

Animals↗

PubMed2001

Influence of a macrolide antibiotic, roxithromycin, on mast cell growth and activation in vitro.

BACKGROUND: Long-term administration of macrolide antibiotics is recognized to be able to favorably modify the clinical condition of inflammatory diseases, such as diffuse panbronchiolitis and cystic fibrosis. However, the precise mechanisms by which macrolide antibiotics could improve clinical conditions of the patients are not well understood. AIM: The present study was designed to examine the influence of macrolide antibiotics on effector cell functions responsible for inflammation through the choice of roxithromycin (RXM) and mast cell. METHODS: Mast cells were induced by long-term culture of splenocytes from BALB/c mice. RXM was added to the cultures at seeding and then every 4-5 days, when the culture medium was replaced with a fresh one. The influence of RXM on mast cell growth was evaluated by counting the number of cells grown on the 16th day. We also examined the influence of RXM on mast cell activation by examining histamine release and inflammatory cytokine secretion. RESULTS AND CONCLUSION: RXM could not inhibit mast cell growth, even when splenocytes were exposed to 100 microg/ml of RXM throughout the entire culture periods. RXM also could not suppress histamine release from cultured mast cells in response to non-immunological and immunological stimulations. However, RXM could suppress inflammatory cytokine, interleukin-1beta, interleukin-6, granulocyte macrophage-colony stimulating factor and tumor necrosis factor-alpha, secretions induced by concanavalin A stimulation at a concentration of as little as 0.5 microg/ml. These results may suggest that RXM modulated the ability of mast cells to secrete inflammatory cytokines and results in improvement of clinical condition of chronic inflammatory diseases.

Animals↗

PubMed2002

Inhibitory action of a macrolide antibiotic, roxithromycin, on co-stimulatory molecule expressions in vitro and in vivo.

OBJECTIVE: The influence of a macrolide antibiotic, roxithromycin (RXM), on co-stimulatory molecule expression was examined in vitro and in vivo. MATERIALS AND METHODS: Spleen cells obtained from BALB/c mice 10 days after immunization with 8.0 microg of hemocyanin absorbed to 4.0 mg of aluminum hydroxide were cultured in the presence of 100.0 microg/ml of hemocyanin and various concentrations of RXM. We first examined the influence of RXM on cell activation by examining the proliferative response of cells and cytokine production. We also examined the influence of RXM on co-stimulatory molecule (CD40, CD80 and CD86) expressions on cultured splenic B-lymphocytes induced by in vitro antigenic stimulation using flow cytometry. In the second part of experiments, non-immunized and immunized mice were treated orally with 2.5 mg/kg of RXM once a day for 4 or 8 weeks. Splenic B lymphocytes were obtained from these mice 24 h after antigenic challenge, and co-stimulatory molecule expressions were examined by flow cytometer. RESULTS: Cell activation induced by in vitro antigenic stimulation was suppressed by RXM when cells were cultured in the presence of more than 5.0 microg/ml of the agent. Addition of RXM at a concentration of 5.0 microg/ml into cell cultures also suppressed co-stimulatory molecule (CD40, CD80 and CD86) expressions on splenic B lymphocytes, which was enhanced by antigenic stimulation in vitro. Oral RXM administration for 4 weeks clearly suppressed the enhancement of CD40 and CD86 (but not CD80) expressions on splenic B lymphocytes induced by antigenic stimulation in vivo. This suppressive activity of RXM on co-stimulatory molecule (CD40 and CD86) expressions was further strengthened by the treatment of mice for 8 weeks. Long-term treatment with oral RXM also suppressed CD80 expressions, which was not suppressed by 4-week treatment. CONCLUSION: The present results suggest that RXM exerts its immunomodulating effects through suppression of both cell activation and co-stimulatory molecule expressions induced by antigenic stimulation. These suppressive activities of RXM might contribute, in part, to the therapeutic mode of action of RXM on inflammatory diseases.

Animals↗

PubMed2004

Suppression of matrix metalloproteinase-9 production from neutrophils by a macrolide antibiotic, roxithromycin, in vitro.

BACKGROUND: Macrolide antibiotics such as erythromycin and roxithromycin (RXM) have an anti-inflammatory effect that may account for their clinical benefit in the treatment of chronic airway inflammatory diseases. However, the precise mechanism of this anti-inflammatory effect is not well understood. PURPOSE: The influence of RXM on matrix metalloproteinase (MMP)-9 production from neutrophils in response to lipopolysaccharide (LPS) stimulation was examined in vitro. METHODS: Neutrophils prepared from normal human peripheral blood (1 x 10(5) cells/ml) were treated with various concentrations of RXM for 1 h, and then stimulated with 1.0 microg/ml of LPS in the presence of the agent for 24 h. MMP-9 and tissue inhibitor of metalloproteinase (TIMP)-1 levels in culture supernatants were examined by enzyme-linked immunosorbent assay. RESULTS: Addition of RXM at more than 5.0 microg/ml into cell cultures caused significant suppression of MMP-9 production, which was increased by LPS stimulation. However, the ability of cells to produce TIMP-1 was not affected by RXM treatment, even when the cells were cultured in the presence of agent at 10.0 microg/mL We then examined the influence of RXM on transcriptional factor, nuclear factor-kappaB and activator protein (AP)-1 activation by LPS stimulation. RXM exerted suppressive action on NF-kappaB (P50 and P65) activation when the cells were cultured for 4 h at more than 5.0 microg/ml of the agent. RXM at more than 2.5 microg/ml also suppressed AP-1 (Fra 1 and Jun B) activation in 4-h cultured cells. We finally examined the influence of RXM on MMP-9 mRNA expression in neutrophils. Addition of RXM into cell cultures at more than 5.0 microg/ml caused significant inhibition of mRNA expression, which was enhanced by LPS stimulation for 12 h. CONCLUSION: These results strongly suggest that RXM inhibits neutrophil transmigration into inflammatory sites and results in favorable modification of the clinical status of inflammatory diseases.

Anti-Bacterial Agents↗

PubMed1999

Suppressive activity of a macrolide antibiotic, roxithromycin, on pro-inflammatory cytokine production in vitro and in vivo.

This study was designed to examine the influence of a macrolide antibiotic, roxithromycin (RXM), on the production of pro-inflammatory cytokines, interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. In the first experiments, we examined the effect of RXM on in vitro cytokine production from lipopolysaccharide (LPS)-stimulated human peripheral blood monocytes. The monocytes were cultured in the presence of various doses of the agent. After 24 h, the culture supernatants were obtained and assayed for IL-1beta and TNF-alpha contents by enzyme-linked immunosorbent assay. RXM suppressed the in vitro production of IL-1beta and TNF-alpha in response to LPS stimulation. This was dose dependent and first noted at a concentration of as little as 0.05 microg/ml, which is much lower than therapeutic blood levels. In the second part of the experiments, we examined the influence of RXM on the appearance of IL-1beta and TNF-alpha in mouse lung extract induced by LPS inhalation. RXM was administered orally into BALB/c mice at a single dose of 2.5 mg/kg once a day for 5-12 weeks. These mice were then instilled with LPS into the trachea and examined for the presence of cytokines in aqueous lung extracts. Pretreatment of mice with RXM for 5 weeks did not influence of the appearance of both IL-1beta and TNF-alpha in aqueous lung extracts. However, pretreatment for more than 7 weeks dramatically suppressed the cytokine appearance in the extracts.

Administration, Inhalation↗

PubMed2005

Mechanism of thymus- and activation-regulated chemokine (TARC)/CCL17 production and its modulation by roxithromycin.

Stimulation with tumor necrosis factor (TNF)alpha and interferon (IFN)gamma synergistically induced thymus- and activation-regulated chemokine (TARC)/CCL17 production from HaCaT keratinocytes (KC). Inhibitors for nuclear factor kappa B (NFkappaB), parthenolide, and Bay 11-7085, and an inhibitor of p38, SB202190, inhibited TNFalpha- and IFNgamma-induced production of CCL17 by HaCaT KC. Surprisingly, an inhibitor of epidermal growth factor receptor tyrosine kinase, PD153035, enhanced the production of CCL17 in HaCaT KC. Roxithromycin (RXM), a 14-membered ring macrolide, suppressed CCL17 production by HaCaT KC induced by IFNgamma and TNFalpha. RXM partially suppressed p38 phosphorylation and NFkappaB-driven luciferase activity induced by TNFalpha and IFNgamma. Degradation of inhibitor of nuclear factor kappa B (IkappaB) alpha upon stimulation with IFNgamma and TNFalpha was not affected by the addition of RXM. Through elucidating the mechanism of CCL17 production, our study indicates that RXM suppresses the production through the inhibition of p38 and NFkappaB, independent of the inhibition of IkappaB degradation.

Anti-Bacterial Agents↗

PubMed2004

Clinical evaluation of roxithromycin: a double-blind, placebo-controlled and crossover trial in patients with acne vulgaris.

We clinically evaluated roxithromycin (ROM) in a double blind, placebo-controlled, and crossover trial in patients with inflammatory acne. Patients with inflammatory acne who were attending our outpatient clinic for treatment and who had not received topical or systemic treatment for the previous month were enrolled in this study. Patients were randomly separated into two groups. Group I consisted of 26 patients. The patients received 2x150 mg/day ROM orally in the first period and 2x1 placebo tablets/day in the second period. Group II consisted of 20 patients. These patients received 2x1 placebo tablets/day in the first period and 2x150 mg/day ROM orally in the second period. The first period was the first four weeks, and then there was a washout period of two weeks (5th and 6th). The second period was the next four weeks (7th to 10th weeks) after the washout period. Median acne scores had clearly decreased in both groups at the end of the study. Differences of median acne scores were statistically significant in both groups between at baseline and at the end of the study (p<0.001). The results showed that ROM is a safe and effective alternative in the treatment of inflammatory acne with few side effects and good compliance.

Acne Vulgaris↗

PubMed1994

[Roxithromycin treatment in patients with chronic lower respiratory tract disease--its clinical efficacy and effect on cytokine].

We demonstrated the efficacy of "long term" roxithromycin (RXM) treatment in 15 patients with chronic lower respiratory tract disease (11 with diffuse panbronchiolitis and 4 with sinobronchial syndrome). (1) Fourteen (93.3%) of the 15 patients showed improvement when assessed by the comprehensive improvement score, and they showed significant improvements in PaO2 (74.2 +/- 10.4 Torr to 84.3 +/- 10.9 Torr, p < 0.01), %VC (86.9 +/- 20.2% to 96.0 +/- 21.9%, p < 0.001) and FEV1 (1.81 +/- 0.87 L to 2.14 +/- 1.08 L, p < 0.01) after RXM treatment. (2) Neutrophils accumulated in the pre-RXM treatment bronchoalveolar lavage (BAL) fluid and decreased in BAL fluid of patients responding to RXM treatment (49.8 +/- 28.3% to 17.1 +/- 15.7%, p < 0.01). Additionally, the levels of interleukin 1 beta and interleukin 8 were significantly higher in BAL fluid of these patients than those in the healthy volunteers (p < 0.025, p < 0.01 respectively), and correlated with the neutrophil accumulation (r = 0.619, p < 0.05). These cytokines showed a decrease after RXM treatment. These results indicated that RXM acts by reducing pulmonary inflammation through reduction of neutrophil migration to inflammatory sites, and is effective on chronic lower respiratory tract disease.

Adult↗