Lipopolysaccharide: Basic Biochemistry, Intracellular Signaling, and Physiological Impacts in the Gut

被引:115
作者
Rhee, Sang Iioon [1 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Div Diegestive Diseases, 675 Charles E Young Dr South, Los Angeles, CA 90095 USA
关键词
Lipopolysaccharides; Toll-like receptors; Inflammatory bowel diseases;
D O I
10.5217/ir.2014.12.2.90
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Lipopolysaccharide (LPS), a main constituent of Gram-negative bacterial membrane, specifically activates Toll-like receptor 4, leading to the production of pleiotropic cytokines/chemokines which in turn regulate inflammatory and innate and subsequent adaptive immune responses. Given that human gut harbors a large collection of commensal bacteria, LPS released by gut microbes is able to make the great impact on gut homeostasis through the intracellular signaling pathways engaged by host-microbial interaction. Emerging evidence indicates that LPS in the gut has a potency to elicit the pathogenesis of intestinal inflammatory diseases such as inflammatory bowel disease and necrotizing enterocolitis. In this review, we discuss the current understanding of the basic biochemistry of LPS, LPS-induced intracellular signaling, and physiological impacts of LPS in the intestine.
引用
收藏
页码:90 / 95
页数:6
相关论文
共 42 条
[21]   Targeting NOX, INOS and COX-2 in inflammatory cells: Chemoprevention using food phytochemicals [J].
Murakami, Akira ;
Ohigashi, Hajime .
INTERNATIONAL JOURNAL OF CANCER, 2007, 121 (11) :2357-2363
[22]   Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways [J].
Murray, Peter J. ;
Smale, Stephen T. .
NATURE IMMUNOLOGY, 2012, 13 (10) :916-924
[23]   Mechanisms of cross hyporesponsiveness to toll-like receptor bacterial ligands in intestinal epithelial cells [J].
Otte, JM ;
Cario, E ;
Podolsky, DK .
GASTROENTEROLOGY, 2004, 126 (04) :1054-1070
[24]   Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice:: Mutations in Tlr4 gene [J].
Poltorak, A ;
He, XL ;
Smirnova, I ;
Liu, MY ;
Van Huffel, C ;
Du, X ;
Birdwell, D ;
Alejos, E ;
Silva, M ;
Galanos, C ;
Freudenberg, M ;
Ricciardi-Castagnoli, P ;
Layton, B ;
Beutler, B .
SCIENCE, 1998, 282 (5396) :2085-2088
[25]   Endotoxin-tolerant mice have mutations in toll-like receptor 4 (Tlr4) [J].
Qureshi, ST ;
Larivière, L ;
Leveque, G ;
Clermont, S ;
Moore, KJ ;
Gros, P ;
Malo, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (04) :615-625
[26]   BIOCHEMISTRY OF ENDOTOXINS [J].
RAETZ, CRH .
ANNUAL REVIEW OF BIOCHEMISTRY, 1990, 59 :129-170
[27]   GRAM-NEGATIVE ENDOTOXIN - AN EXTRAORDINARY LIPID WITH PROFOUND EFFECTS ON EUKARYOTIC SIGNAL TRANSDUCTION [J].
RAETZ, CRH ;
ULEVITCH, RJ ;
WRIGHT, SD ;
SIBLEY, CH ;
DING, AH ;
NATHAN, CF .
FASEB JOURNAL, 1991, 5 (12) :2652-2660
[28]   Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis [J].
Rakoff-Nahoum, S ;
Paglino, J ;
Eslami-Varzaneh, F ;
Edberg, S ;
Medzhitov, R .
CELL, 2004, 118 (02) :229-241
[29]   Murine TOLL-like receptor 4 confers lipopolysaccharide responsiveness as determined by activation of NFκB and expression of the inducible cyclooxygenase [J].
Rhee, SH ;
Hwang, D .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (44) :34035-34040
[30]   BACTERIAL-ENDOTOXINS [J].
RIETSCHEL, ET ;
BRADE, H .
SCIENTIFIC AMERICAN, 1992, 267 (02) :54-61