Differential effects of amphotericin B and liposomal amphotericin B on inflammatory cells in vitro

Baronti, Roberto; Masini, Emanuela; Bacciottini, Lucia; Mannaioni, P. F.

doi:10.1007/pl00000302

Cited by 7 publications

(4 citation statements)

References 16 publications

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“…In addition, we have found that the significant increase of histamine release precedes that of degranulation or LDH release. Baronti et al (2002) have reported that sodium deoxycholate induces isolated mast cells to release histamine and that this is accompanied by LDH release, whereas at a low concentration of sodium deoxycholate, the increase of histamine release is more notable than that of LDH. This earlier increase of histamine release may indicate the greater sensitivity of histamine release as an indicator of degranulation, although further study is needed to establish this effect.…”

Section: Discussionmentioning

confidence: 94%

Effect of oxygen–glucose deprivation on degranulation and histamine release of mast cells

Shen

Dai

et al. 2005

Cell Tissue Res

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The purpose of this study was to investigate the effect of oxygen-glucose deprivation (OGD) on degranulation and histamine release of mast cells. Cultured mast cells were exposed to OGD for 1, 2, 4, 8, or 16 h. At 2 h of OGD exposure, the degranulation percentage of mast cells had increased and subsequently showed a progressive further increase, associated with a similar change in lactate dehydrogenase release. Histamine release increased significantly from 1 h of OGD exposure. These results indicate that OGD induces mast cells to degranulate, possibly via a cytotoxic response. This in vitro ischemic model of mast cells might clarify their roles in the pathological processes induced by cerebral ischemia.

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Section: Discussionmentioning

confidence: 94%

Effect of oxygen–glucose deprivation on degranulation and histamine release of mast cells

Shen

Dai

et al. 2005

Cell Tissue Res

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“…Consistent with this clinical observation are the findings that amphotericin B deoxycholate induces histamine release from rat serosal mast cells and human basophils [75]. This effect may be due to IgE recognition of micellar complexes with deoxycholate, because such effect was not observed with pure and liposomal amphotericin B or in a human mast cell line lacking IgE [76].…”

Section: Infusion-related Toxicitymentioning

confidence: 53%

Defining Targets for Investigating the Pharmacogenomics of Adverse Drug Reactions to Antifungal Agents

2008

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Adverse drug reactions (ADRs) associated with antifungal therapy are major problems in patients with invasive fungal infections. Whether by clinical history or patterns of genetic variation, the identification of patients at risk for ADRs should result in improved outcomes while minimizing deleterious side effects. A major contributing factor to ADRs with antifungal agents relates to drug distribution, metabolism and excretion. Genetic variation in key genes can alter the structure and expression of genes and gene products (e.g., proteins). Thus far, the effort has focused on identifying polymorphisms with either empirical or predicted in silico functional consequences; the best candidate genes encode phase I and II drug-metabolizing enzymes (e.g., CYP2C19 and N-acetyltransferase), plasma proteins (albumin and lipoproteins) and drug transporters (P-glycoprotein and multidrug resistance proteins), which can affect the disposition of antifungal agents, eventually leading to dose-dependent (type A) toxicity. Less is known regarding the key genes that interact with antifungal agents, resulting in idiosyncratic (type B) ADRs. The possible role of certain gene products and genetic polymorphisms in the toxicities of antifungal agents are discussed in this review. The preliminary data address the following: low-density lipoproteins and cholesteryl ester transfer protein in amphotericin B renal toxicity; toll-like receptor 1 and 2 in amphotericin B infusion-related ADRs; phosphodiesterase 6 in voriconazole visual adverse events; flavin-containing monooxygenase, glutathione transferases and multidrug resistance proteins 1 and 2 in ketoconazole and terbinafine hepatotoxicity; CYP enzymes and P-glycoprotein in drug interactions between azoles and coadministered medications; multidrug resistance proteins 8 and 9 on 5-flucytosine bone marrow toxicity; and mast cell activation in caspofungin histamine release. This will focus on high-priority candidate genes, which could provide a starting point for molecular studies to elucidate the potential mechanisms for understanding toxicity associated with antifungal drugs as well as identifying candidate genes for large population prospective genetic association studies.

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“…Our findings are inconsistent with those of a previous report of histamine release secondary to amphotericin B deoxycholate exposure. 13 The investigators found that amphotericin B deoxycholate induced not only cytotoxic histamine release but also a sustained increase in CD63 expression in both rat serosal mast cells and human basophils. Such effects were not observed in response to pure or liposomal amphotericin B, suggesting that the histamine release observed was due to the micellar complexes with deoxycholate.…”

Section: Discussionmentioning

confidence: 99%

Effects of Amphotericin B and Caspofungin on Histamine Expression

et al. 2003

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Amphotericin B deoxycholate does not affect histamine concentrations or histamine N-methyltransferase activity in whole blood or HMC-1 cells, suggesting that the amphotericin B-induced infusion-related reaction is not a histamine-mediated event. Conversely, caspofungin increased histamine concentrations in whole blood and HMC-1 cells and inhibited histamine N-methyltransferase activity. These data suggest that infusion-related reactions associated with caspofungin may be mediated by histamine release secondary to caspofungin.

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Differential effects of amphotericin B and liposomal amphotericin B on inflammatory cells in vitro

Cited by 7 publications

References 16 publications

Effect of oxygen–glucose deprivation on degranulation and histamine release of mast cells

Effect of oxygen–glucose deprivation on degranulation and histamine release of mast cells

Defining Targets for Investigating the Pharmacogenomics of Adverse Drug Reactions to Antifungal Agents

Effects of Amphotericin B and Caspofungin on Histamine Expression

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