Linked Life Data

15856892

Source:http://linkedlifedata.com/resource/pubmed/id/15856892

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-4-28
pubmed:abstractText
The effects of a water-soluble amphotericin B (AmB)-arabinogalactan (AG) conjugate on several immune functions were investigated. The experiments measured the effects of AmB-AG on (1) release of tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO), and interferon-gamma (IFN-gamma) from phagocytic cells and (2) cell-mediated immune responses. AmB-AG increased TNF-alpha release from mouse peritoneal macrophages and human monocytes but had no effect on IFN-gamma and NO release. A commercial preparation of nonconjugated AmB (Fungizone) also increased TNF-alpha production, but to a lesser extent than AmB-AG. AG alone had no effect on TNF-alpha production, proving that AmB caused the increased TNF-alpha production. AmB-AG and Fungizone were also tested for their effect on B- and T-cell proliferation. Neither compound altered T-lymphocyte responses to concanavalin A, but both inhibited the stimulation of B lymphocytes by lipopolysaccharides. However, Fungizone showed a stronger inhibitory effect on B cells. Allocytotoxicity was also inhibited by AmB-AG and more strongly by Fungizone. The increased production of TNF-alpha by cells treated with AmB-AG and the lower inhibitory effect of AmB-AG on lymphocyte stimulation and allocytotoxicity, as compared with Fungizone, explain the better therapeutic efficacy of the AmB-polysaccharide conjugate. AmB is active because of its preferential binding to ergosterol rather than cholesterol, the former sterol preferentially present in parasite surface membranes. This is also valid for the axenic amastigotes, which were sensitive to the AmB-AG. Overall, our results suggest that the antileishmanial activity of AmB-AG is mediated both directly and via modulation of immune functions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3395
pubmed:author
pubmed:issnType
Print
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
158-63
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15856892-Amphotericin B, pubmed-meshheading:15856892-Animals, pubmed-meshheading:15856892-Antiprotozoal Agents, pubmed-meshheading:15856892-B-Lymphocytes, pubmed-meshheading:15856892-Biological Assay, pubmed-meshheading:15856892-Galactans, pubmed-meshheading:15856892-Humans, pubmed-meshheading:15856892-Immunity, Cellular, pubmed-meshheading:15856892-Interferon-gamma, pubmed-meshheading:15856892-Leishmania tropica, pubmed-meshheading:15856892-Luminescent Measurements, pubmed-meshheading:15856892-Lymphocyte Activation, pubmed-meshheading:15856892-Macrophages, Peritoneal, pubmed-meshheading:15856892-Mice, pubmed-meshheading:15856892-Mice, Inbred BALB C, pubmed-meshheading:15856892-Mice, Inbred ICR, pubmed-meshheading:15856892-Monocytes, pubmed-meshheading:15856892-Nitric Oxide, pubmed-meshheading:15856892-Reactive Oxygen Species, pubmed-meshheading:15856892-T-Lymphocytes, pubmed-meshheading:15856892-Tumor Necrosis Factor-alpha
pubmed:year
2005
pubmed:articleTitle
The effect of amphotericin b derivatives on Leishmania and immune functions.
pubmed:affiliation
Department of Medicinal Chemistry, School of Pharmacy, Hebrew University of Jerusalem, Jerusalem 91120, Israel.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't