Treatment of Intra-Abdominal Abscesses Caused by<i>Candida albicans</i>with Antifungal Agents and Recombinant MurineGranulocyte Colony-StimulatingFactor

Vonk, Alieke G.; Netea, Mihai G.; Krieken, J. Han van; Verweij, Paul E.; Meer, J.W.M. van der; Kullberg, Bart Jan

doi:10.1128/aac.47.12.3688-3693.2003

Cited by 8 publications

(11 citation statements)

References 25 publications

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“…A similar beneficial effect of G-CSF was found in an intra-abdominal abscess mouse model caused by C. albicans, in which modulation of host defense with G-CSF prophylaxis significantly reduced the number of Candida c.f.u. in intra-abdominal abscesses [114]. Moreover, in the same study, prophylactic administration of G-CSF followed by antifungal treatment showed a tendency towards more efficient C. albicans reduction within the abscesses than antifungal treatment alone [114].…”

Section: Candidiasismentioning

confidence: 92%

“…Consistent with its ability to increase neutrophil number, influx and activation into infected sites [65], G-CSF has been shown to beneficially influence the course of acute disseminated candidiasis in both immunocompetent [112][113][114][115] and neutropenic mice [116,117]. Immunocompetent CBA mice treated with prophylactic recombinant murine G-CSF showed reduced mortality rate and fungal outgrowth in the liver and spleen during disseminated candidiasis compared with untreated animals, which was associated with increased influx of neutrophils at the site of infection and increased production of oxygen radicals [112].…”

Section: Candidiasismentioning

confidence: 99%

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Therapeutic Modulation of Cytokines in Chronic Infectious Diseases

Villar¹,

Dongari-Bagtzoglou²

2006

CPD

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The recent increase in immunocompromised patient populations, including HIV-infected patients, cancer patients with chemotherapy-induced neutropenia, and transplant recipients receiving immunosuppressive therapy, has led to an increased incidence of clinically significant chronic opportunistic infections. Traditional treatment of chronic persistent infections has strongly relied on the use of antimicrobial drugs. However, unsatisfactory results with drug monotherapy and emergence of resistant strains have prompted the use of adjunctive cytokine therapies for the treatment of these infections. During the past decade, a wide spectrum of immunomodulators has been tested in human clinical trials and animal models of chronic infections caused by a variety of bacteria, fungi, viruses and parasites. This review compiles recent information on advances in the use of cytokines as a therapeutic strategy in chronic bacterial, parasitic, fungal and viral infections.

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Section: Candidiasismentioning

confidence: 92%

Section: Candidiasismentioning

confidence: 99%

Therapeutic Modulation of Cytokines in Chronic Infectious Diseases

Villar¹,

Dongari-Bagtzoglou²

2006

CPD

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“…In neutropenic mice, administration of recombinant human G-CSF increases leukocyte number and protects against C. albicans [18]. Prophylaxis with G-CSF also protects against intra-abdominal Candida abscesses, but once infection has developed, the additional benefi t of G-CSF to administration of effective antifungal chemotherapy is unclear [19]. The role of peg-G-CSF was evaluated in non-neutropenic mice with candidiasis.…”

Section: Candidiasismentioning

confidence: 99%

“…Both classes of CSF have been evaluated in preclinical studies for prevention, and as adjuncts, for treatment of multiple fungal infections, including candidiasis, aspergillosis, mucormycosis, and cryptococcosis [4, 15,16,[18][19][20][21][22]. Both CSFs are widely used for prevention of invasive infections in patients with neutropenia.…”

Section: Overviewmentioning

confidence: 99%

Augmentation of innate host defenses against opportunistic fungal pathogens

Shoham¹,

Roilides²,

Walsh

2009

Curr Fungal Infect Rep

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Development of invasive fungal infection is the result of the complex interaction between fungal and host factors. The outcome of infection, once it has developed, depends upon appropriate use of antifungal therapy, surgical debridement as indicated, and improvement of host defenses. Thus, there have been major efforts for development of new strategies for immunomodulation and augmentation of host defenses in prevention and treatment of invasive mycoses. These modalities include granulocyte and granulocyte-macrophage colony-stimulating factors, interferon-γ, granulocyte transfusions, immunotherapy with infusion of dendritic cells and T cells, anti-heat shock protein 90 monoclonal antibodies, long pentraxin 3, mannose-binding lectin, and deferasirox. Although major strides in our understanding of augmentation of host response to invasive fungal infections are opening up novel avenues of therapy to harness patients' innate immune systems against these frequently lethal pathogens, well-designed clinical trials are needed to demonstrate safety and effi cacy of these new approaches.

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“…However, except for a minor beneficial influence of G-CSF on established Candida abscesses (27), no data are available regarding the influence of G-CSF on established mixed bacterial abscesses.…”

mentioning

confidence: 99%

Effect of Recombinant Murine Granulocyte Colony-Stimulating Factor with or without Fluoroquinolone Therapy on Mixed-Infection Abscesses in Mice

Stearne¹,

Vonk

Kullberg

et al. 2005

Antimicrob Agents Chemother

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The aim of the study was to determine if immunomodulation of host defense with recombinant murine granulocyte colony-stimulating factor (G-CSF) improves the efficacy of trovafloxacin or moxifloxacin in abscesses containing Bacillus fragilis ATCC 23745 and different Escherichia coli strains varying in virulence. Treatment of mice inoculated with 10 7 CFU B. fragilis and 10 5 CFU low-virulence E. coli with either trovafloxacin (150 mg/kg/day every 24 hours, days 3 to 7) or moxifloxacin (96 mg/kg/day every 12 hours, days 3 to 7), significantly reduced the number of B. fragilis to 6.9 ؎ 0.35 and 5.8 ؎ 0.10 and that of E. coli to 4.9 ؎ 0.09 and 4.2 ؎ 0.07 log CFU/abscess for trovafloxacin and moxifloxacin, respectively, compared to controls (B. fragilis 8.7 and E. coli 7.4 log CFU/abscess) on day 8. Also, moxifloxacin was more potent than trovafloxacin. Addition of G-CSF prophylaxis (1 g once on day ؊1) or therapy (1 g/day on days 3 to 7) to fluoroquinolone treatment did not improve the efficacy of fluoroquinolone therapy alone. The effect of moxifloxacin with or without G-CSF prophylaxis on abscesses with a virulent hemolytic E. coli strain was also studied. In moxifloxacin-treated mice, 75% survived infection compared to 10% of controls. Combining moxifloxacin with G-CSF prophylaxis significantly decreased survival (30%) compared to moxifloxacin alone. In addition, G-CSF prophylaxis resulted in a threefold (E. coli) to 100-fold (B. fragilis) increased outgrowth in the abscesses of surviving mice. In conclusion, the addition of G-CSF to a fluoroquinolone is not advisable since, depending on the virulence of the E. coli strains, this might detrimentally influence the outcome of therapy.

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Treatment of Intra-Abdominal Abscesses Caused byCandida albicanswith Antifungal Agents and Recombinant MurineGranulocyte Colony-StimulatingFactor

Cited by 8 publications

References 25 publications

Therapeutic Modulation of Cytokines in Chronic Infectious Diseases

Therapeutic Modulation of Cytokines in Chronic Infectious Diseases

Augmentation of innate host defenses against opportunistic fungal pathogens

Effect of Recombinant Murine Granulocyte Colony-Stimulating Factor with or without Fluoroquinolone Therapy on Mixed-Infection Abscesses in Mice

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