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Effects of bile salts and aliphatic ionic surfactants on human lymphocyte proliferation
Author(s) -
Podevin P.,
Correia L.,
Montet J C.,
Conti F.,
Chéreau C.,
Calmus Y.,
Poupon R.
Publication year - 2001
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2001.00778.x
Subject(s) - chemistry , mixed lymphocyte reaction , critical micelle concentration , lymphocyte , bromide , steroid , amphiphile , bilayer , in vitro , membrane , cell , micelle , lipid bilayer , intracellular , biophysics , biochemistry , aqueous solution , organic chemistry , immune system , t cell , immunology , biology , polymer , copolymer , hormone
Background The molecular mechanisms involved in the immunosuppressive properties of bile salts are partly unknown. Methods The aim of the study was to compare the effects of bile salts to those of various compounds with a steroid structure, or straight‐chain hydrocarbons of different lengths and polar groups in the human mixed lymphocyte reaction. Results We showed a significant correlation between the effects of bile salts and a low critical micellar concentration, a high surface activity index, and the absence of conjugation. In addition to mixed lymphocyte reaction (MLR) inhibition, chenodeoxycholate (CDC) inhibit ConA‐induced IL2 production without any effect on IL2 R expression. Fusidate, a negatively charged steroid, with physical properties comparable to those of deoxycholate, had similar effects. Cetyltrimethylammonium bromide (CTAB), which exhibited a very low critical micellar concentration, inhibited mixed lymphocyte reaction in an extent comparable to cyclosporin A. In contrast, aliphatic compounds with critical micellar concentrations in the same range as bile salts but with a lower molecular area had no effect. Conclusion Amphiphilic negatively charged molecules inhibit T‐cell proliferation to an extent that is dependent upon their hydrophobicity. These results may be explained, at least in part, by a modification in the cell membrane lipid bilayer structure.