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Hydrolysis of thalidomide abrogates its ability to enhance mononuclear cell synthesis of IL-2 as well as its ability to suppress the synthesis of TNF-α by E.J Shannon; Felipe Sandoval; James L. Krahenbuhl is a Immunology and Microbiology article available to read on EtoBox.

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Thalidomide is effective in the treatment of inflammatory conditions like erythema nodosum leprosum in leprosy patients, and aphthous ulcers in AIDS patients. Its mechanism of action is uncertain and reports of its effect on the synthesis of inflammatory cytokines such as IL-2 and TNF-a are contradictory. As thalidomide is labile to spontaneous hydrolysis at pH 7.4, studies were carried out to explore the effects of deliberate hydrolysis on the ability of thalidomide to modulated Ž .Ž . cytokine production by human mononuclear cells stimulated in vitro with Staphylococcal enterotoxin A SEA IL-2 or Ž .Ž . lipopolysaccharide from Salmonella minnesota LPS TNF-a . Unhydrolyzed thalidomide at 4.0 mgrml consistently enhanced the synthesis of IL-2 in SEA-stimulated cells, and suppressed the synthesis of TNF-a in LPS-stimulated cells; whereas, hydrolyzed thalidomide had no enhancing effect on SEA stimulated-cell synthesis of IL-2 or suppressive effect on LPS stimulated-cell synthesis of TNF-a. These findings demonstrate that thalidomide's ability in vitro to enhance IL-2 and to suppress TNF-a in stimulated cells is dependent on the intact molecule and underscore the necessity to employ tha

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Author

E.J Shannon; Felipe Sandoval; James L. Krahenbuhl

Publisher

Elsevier Science; Elsevier ; Elsevier BV (ISSN 0162-3109)

Published

1997

Language

EN

Field

Immunology and Microbiology (Life Sciences)