ArticleAntimicrobial agents and chemotherapy2001
Reduction of no synthase expression and tumor necrosis factor alpha production in macrophages by amphotericin B lipid carriers.
Article in Antimicrobial agents and chemotherapy, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- "Click" amphotericin B in prodrug nanoformulations for enhanced systemic fungemia treatment.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Supplementation of host response by targeting nitric oxide to the macrophage cytosol is efficacious in the hamster model of visceral leishmaniasis and adds to efficacy of amphotericin B.International journal for parasitology. Drugs and drug resistance · 2016Article
- A curative immune profile one week after treatment of Indian kala-azar patients predicts success with a short-course liposomal amphotericin B therapy.PLoS neglected tropical diseases · 2010Article
- Antiproliferative Properties of Type I and Type II Interferon.Pharmaceuticals (Basel, Switzerland) · 2010Article
- Optimizing efficacy of Amphotericin B through nanomodification.International journal of nanomedicine · 2007Review
- Real-time reverse transcription-PCR quantification of cytokine mRNA expression in golden Syrian hamster infected with Leishmania infantum and treated with a new amphotericin B formulation.Antimicrobial agents and chemotherapy · 2006Article
- Toxicity and antileishmanial activity of a new stable lipid suspension of amphotericin B.Antimicrobial agents and chemotherapy · 2003Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study compared the abilities of different lipid carriers of amphotericin B (AMB) to activate murine peritoneal macrophages, as assessed by their capacities to produce nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha). Although AMB alone did not induce NO production, synergy was observed with gamma interferon but not with lipopolysaccharide. This synergy could not be explained by the mobilization of the nuclear activation factor NF-kappaB by AMB. On the other hand, AMB induced TNF-alpha production without a costimulator and no synergy was observed. Anti-TNF-alpha antibodies did not influence NO production, and an inhibitor of NO synthase did not affect TNF-alpha production, indicating that the production of one of these effector molecules was independent of that of the other. The incorporation of AMB into lipid carriers reduced NO and TNF-alpha production with all formulations but more so with liposomes than with lipid complexes. NO production was correlated with the induction of NO synthase II, revealed by Western blotting. The extent of association of AMB with macrophages depended on the formulation, especially on the AMB/lipids ratio: the higher the ratio was, the greater the AMB association with macrophages. However, there was no clear correlation between AMB association with macrophages, whether internalized or bound to the membrane, and immunostimulating effects. These results may explain the reduced toxicities of lipid-based formulations of AMB.
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