IMMUNOMODULATORY SPECTRUM OF LIPIDS ASSOCIATED WITH MYCOBACTERIUM-AVIUM SEROVAR-8

被引:33
作者
BARROW, WW
DAVIS, TL
WRIGHT, EL
LABROUSSE, V
BACHELET, M
RASTOGI, N
机构
[1] UNIV N TEXAS, DEPT BIOL, DENTON, TX 76203 USA
[2] INST PASTEUR, UNITE TB & MYCOBACTERIES, F-75724 PARIS, FRANCE
[3] INST PASTEUR, UNITE PHARMACOL CELLULAIRE, F-75724 PARIS, FRANCE
[4] SO RES INST, MYCOBACTERIOL RES UNIT, BIRMINGHAM, AL 35255 USA
[5] INST PASTEUR, TB & MYCOBACTERIES UNITE, F-97165 POINTE A PITRE, Guadeloupe, FRANCE
关键词
D O I
10.1128/IAI.63.1.126-133.1995
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Lipid fractions obtained from Mycobacterium avium serovar 8 were assessed for the ability to affect various immune functions of human peripheral blood mononuclear cells (PBM). Lipids included a total lipid fraction and fractions eluted from silicic acid column separation of that total lipid fraction, using chloroform and chloroform methanol combinations. Lipid fractions were assayed for total carbohydrate and total 6-deoxyhexose content and were assessed for the ability to influence human macrophage function and the capacity to induce secretion of prostaglandin E(2) (PGE(2)) and tumor necrosis factor alpha in PBM. The total lipid and serovar-specific glycopeptidolipid (GPL) fractions both induced significant levels of tumor necrosis factor alpha, as well as PGE(2), in PBM exposed to a sublethal concentration of 100 mu g lipid per 2 x 10(6) cells. In addition, the same concentrations of the 5 to 7% and GPL fractions induced significant levels of leukotriene B4 in PBM. Comparison of carbohydrate and 6-deoxyhexose contents of each fraction suggested a relationship to carbohydrate content and ability of fractions to induce immune modulator secretion, Analysis of GPL fractions from ill. avium serovars 4 and 20 revealed that those GPL lacked the ability to induce PGE,, These results are explained by considering the difference in the carbohydrate residues of the oligosaccharide moieties.
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页码:126 / 133
页数:8
相关论文
共 58 条
[21]  
FERRERI NR, 1992, J BIOL CHEM, V267, P9443
[22]   PROSTAGLANDIN-E2 INHIBITS THE RELEASE OF TUMOR-NECROSIS-FACTOR-ALPHA, RATHER THAN INTERLEUKIN-1-BETA, FROM HUMAN MACROPHAGES [J].
FIEREN, MWJA ;
VANDENBEMD, GJCM ;
BENEFRAIM, S ;
BONTA, IL .
IMMUNOLOGY LETTERS, 1992, 31 (01) :85-90
[23]   TUMOR NECROSIS FACTOR-INDUCED MORTALITY IS REVERSED WITH CYCLOOXYGENASE INHIBITION [J].
FLETCHER, JR ;
COLLINS, JN ;
GRAVES, ED ;
LUTERMAN, A ;
WILLIAMS, MD ;
IZENBERG, SD ;
RODNING, CB .
ANNALS OF SURGERY, 1993, 217 (06) :668-675
[24]   COMPARISON OF INVITRO-CELL CYTO-TOXIC ASSAYS FOR TUMOR NECROSIS FACTOR [J].
FLICK, DA ;
GIFFORD, GE .
JOURNAL OF IMMUNOLOGICAL METHODS, 1984, 68 (1-2) :167-175
[25]   LEUKOTRIENES AND MACROPHAGE ACTIVATION - AUGMENTED CYTO-TOXIC ACTIVITY AND ENHANCED INTERLEUKIN-1, TUMOR NECROSIS FACTOR AND HYDROGEN-PEROXIDE PRODUCTION [J].
GAGNON, L ;
FILION, LG ;
DUBOIS, C ;
ROLAPLESZCZYNSKI, M .
AGENTS AND ACTIONS, 1989, 26 (1-2) :141-147
[26]  
GOLDMAN G, 1993, SURGERY, V113, P297
[27]  
Goren M.B., 1979, TUBERCULOSIS, P63
[28]   TUMOR-NECROSIS-FACTOR-ALPHA POTENTIATES PHOSPHOLIPASE A2-STIMULATED RELEASE AND METABOLISM OF ARACHIDONIC-ACID IN CULTURED INTESTINAL EPITHELIAL-CELLS (INT-407) [J].
GUSTAFSONSVARD, C ;
TAGESSON, C ;
BOLL, RM ;
KALD, B .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1993, 28 (04) :323-330
[29]   INVOLVEMENT OF PROSTAGLANDIN-PRODUCING PATHWAY IN THE CYTOTOXIC ACTION OF TUMOR-NECROSIS-FACTOR [J].
HAYAKAWA, M ;
OKU, N ;
TAKAGI, T ;
HORI, T ;
SHIBAMOTO, S ;
YAMANAKA, Y ;
TAKEUCHI, K ;
TSUJIMOTO, M ;
ITO, F .
CELL STRUCTURE AND FUNCTION, 1991, 16 (04) :333-340
[30]  
Hooper L C, 1988, Adv Exp Med Biol, V239, P309