Local and systemic effects of macrophage cytokines in intestinal inflammation

被引:25
作者
Murch, SH [1 ]
机构
[1] Univ London Royal Free Hosp, Dept Paediat Gastroenterol, London NW3 2QG, England
关键词
inflammatory bowel disease; cytokines; TNF-alpha; IL-1; IL-6; growth;
D O I
10.1016/S0899-9007(98)00083-5
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
The activation of macrophages and newly recruited monocytes appears to be common to both Crohn's disease and ulcerative colitis, despite different inductive stimuli. Similar activation occurs acutely during the course of invasive intestinal infections such as shigellosis, but is then usually downregulated. The macrophage cytokines tumor necrosis factor-ct and interleukin-l IL-1, are centrally involved in the local inflammatory response, and blockade of either cytokine greatly attenuates the inflammatory lesion. Induction of focal vascular thrombosis and matrix degradation are thought to be an important component of this focal damage. Both cytokines and IL-6 are now recognized to contribute to the systemic effects of intestinal disease, including growth suppression, anorexia, and chronic anemia. Disturbance of sleep patterns, mood, and affect may also occur, and recent evidence points towards bidirectional interplay between macrophage cytokines and central nervous system function. (C) Elsevier Science Inc. 1998.
引用
收藏
页码:780 / 783
页数:4
相关论文
共 38 条
[1]   STIMULATION OF BONE-RESORPTION AND INHIBITION OF BONE-FORMATION INVITRO BY HUMAN-TUMOR NECROSIS FACTORS [J].
BERTOLINI, DR ;
NEDWIN, GE ;
BRINGMAN, TS ;
SMITH, DD ;
MUNDY, GR .
NATURE, 1986, 319 (6053) :516-518
[2]  
BROWN SL, 1987, J IMMUNOL, V139, P3181
[3]   INTERLEUKIN-6 IS THE MAJOR REGULATOR OF ACUTE PHASE PROTEIN-SYNTHESIS IN ADULT HUMAN HEPATOCYTES [J].
CASTELL, JV ;
GOMEZLECHON, MJ ;
DAVID, M ;
ANDUS, T ;
GEIGER, T ;
TRULLENQUE, R ;
FABRA, R ;
HEINRICH, PC .
FEBS LETTERS, 1989, 242 (02) :237-239
[4]  
CHAPLIN DD, 1992, TUMOR NECROSIS FACTO, P197
[5]   ROLE OF TUMOR NECROSIS FACTOR-ALPHA IN THE PATHOPHYSIOLOGIC ALTERATIONS AFTER HEPATIC ISCHEMIA REPERFUSION INJURY IN THE RAT [J].
COLLETTI, LM ;
REMICK, DG ;
BURTCH, GD ;
KUNKEL, SL ;
STRIETER, RM ;
CAMPBELL, DA .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (06) :1936-1943
[6]   RECOMBINANT INTERLEUKIN-1 RECEPTOR ANTAGONIST BLOCKS THE PROINFLAMMATORY ACTIVITY OF ENDOGENEOUS INTERLEUKIN-1 IN RABBIT IMMUNE COLITIS [J].
COMINELLI, F ;
NAST, CC ;
DUCHINI, A ;
LEE, M .
GASTROENTEROLOGY, 1992, 103 (01) :65-71
[7]   Interleukin 6 causes growth impairment in transgenic mice through a decrease in insulin-like growth factor-I - A model for stunted growth in children with chronic inflammation [J].
DeBenedetti, F ;
Alonzi, T ;
Moretta, A ;
Lazzaro, D ;
Costa, P ;
Poli, V ;
Martini, A ;
Ciliberto, G ;
Fattori, E .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (04) :643-650
[8]  
DUNN AJ, 1996, PHYSL IMMUNITY, P145
[9]   TISSUE-SPECIFIC REGULATION OF GUINEA-PIG LIPOPROTEIN-LIPASE - EFFECTS OF NUTRITIONAL STATE AND OF TUMOR NECROSIS FACTOR ON MESSENGER-RNA LEVELS IN ADIPOSE-TISSUE, HEART AND LIVER [J].
ENERBACK, S ;
SEMB, H ;
TAVERNIER, J ;
BJURSELL, G ;
OLIVECRONA, T .
GENE, 1988, 64 (01) :97-106
[10]   RECOMBINANT TUMOR-NECROSIS-FACTOR DEPRESSES CYTOCHROME P450-DEPENDENT MICROSOMAL DRUG-METABOLISM IN MICE [J].
GHEZZI, P ;
SACCARDO, B ;
BIANCHI, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1986, 136 (01) :316-321