Abstract.
Background: Formulations of amphotericin include a deoxycholate suspension (d-Amph), an amphotericin-B lipid complex (Ablc), and a liposomal product (L-Amph). Fever is most frequent with d-Amph, intermediate with Ablc, and lowest with L-Amph.
Objective: To determine if the release of tumor necrosis factor-alpha (TNF-α) and interleukin-1-beta (IL-1) from brain endothelium corresponds to the incidence of amphotericin fever.
Results: Release of TNF-α and IL-1β after L-Amph treatment was similar to negative controls while after d-Amph treatment release was similar to lipopolysaccharide. Ablc treatment produced intermediate pyrogen release.
NF-κB expression, a transcriptional regulator for TNF-α and IL-1β genes, corresponded to this secretion pattern. TNF-α release was elevated 2 hours (p = 0.0021) after treatment while significant elevations in IL-1β required 6 hours (p = 0.0009).
Conclusion: Results from this in vitro study suggest that amphotericin fever may be directly mediated by brain endothelium. These experiments also suggest that amphotericin fever is initially mediated by TNF-α.
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Received 7 March 2005; returned for revision 27 May 2005; accepted by G. Geisslinger 24 June 2005
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McGuire, T.R., Trickler, W.J., Smith, L. et al. Release of TNF-α and IL-1β from porcine brain endothelium corresponds to the pyrogenic potential of three marketed formulations of amphotericin. Inflamm. res. 54, 375–379 (2005). https://doi.org/10.1007/s00011-005-1370-9
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DOI: https://doi.org/10.1007/s00011-005-1370-9