Mechanism of pentoxifylline mediated down-regulation of killer lineage cell functionsReport as inadecuate




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Mediators of Inflammation - Volume 2 1993, Issue 5, Pages 379-384

Research paper

Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, P.O. Box 3354, Riyadh 11211, Saudi Arabia

Department of Oncology, King Faisal Specialist Hospital and Research Centre, P.O. Box 3354, Riyadh 11211, Saudi Arabia

Department of Pathology, King Faisal Specialist Hospital and Research Centre, P.O. Box 3354, Riyadh 11211, Saudi Arabia

Received 22 June 1993; Accepted 9 August 1993

Copyright © 1993 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The authors reported recently that endotoxaemia mediated elevated levels of tumour necrosis factor TNF-α and interleukin-1α IL-1α were involved in the pathophysiology of acute heat stroke patients. Pentoxifylline PTX is known to modulate neutrophil functions. In the present study the effects of PTX on lipopolysaccharide LPS and cytokine induced T-cell and macrophage ΦM activation, and on natural killer NK cell and lymphokine activated killer LAK cell mediated cytotoxicity were examined. Finally, the effect of PTX on the expression of adhesion molecules LFA-1, Mac-1 and ICAM-1, and cytokine IL-1α, IL-2, TNF-α, IL-6 and IFN-γ production and their surface receptor expression in response to LPS activation was investigated. PTX free cultures served as a control. Results revealed that PTX can down-regulate all the above-mentioned immunological parameters in a dosedependent manner. These findings might have far reaching clinical implications.





Author: R. S. Parhar, P. Ernst, K. Sheth, M. Einspenner, and S. Al-Sedairy

Source: https://www.hindawi.com/



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