Mechanism of cytokine modulation of epithelial tight junction barrier

被引:507
作者
Al-Sadi, Rana [1 ]
Boivin, Michel [1 ]
Ma, Thomas [1 ,2 ]
机构
[1] Univ New Mexico, Sch Med, Dept Internal Med, Mail Stop Code 10 5550, Albuquerque, NM 87131 USA
[2] Albuquerque Vet Affairs Med Ctr, Albuquerque, NM 87108 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷
关键词
Tight Junctions; Cytokines; Intestinal Epithelial Cells; Barrier Function; Inflammation; Review; TUMOR-NECROSIS-FACTOR; INFLAMMATORY-BOWEL-DISEASE; TOTAL PARENTERAL-NUTRITION; EPIDERMAL-GROWTH-FACTOR; CACO-2 CELL MONOLAYERS; ALPHA TNF-ALPHA; NF-KAPPA-B; INTERFERON-GAMMA; IFN-GAMMA; INTESTINAL PERMEABILITY;
D O I
10.2741/3413
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cytokines play a crucial role in the modulation of inflammatory response in the gastrointestinal tract. Pro-inflammatory cytokines including tumor necrosis factor-alpha, interferon-gamma, interleukin-1 beta (IL-1 beta), and interleukin-12 are essential in mediating the inflammatory response, while anti-inflammatory cytokines including interleukin-10 and transforming growth factor-beta are important in the attenuation or containment of inflammatory process. It is increasingly recognized that cytokines have an important physiological and pathological effect on intestinal tight junction (TJ) barrier. Consistent with their known pro-inflammatory activities, pro-inflammatory cytokines cause a disturbance in intestinal TJ barrier, allowing increased tissue penetration of luminal antigens. Recent studies indicate that the inhibition of cytokine induced increase in intestinal TJ permeability has an important protective effect against intestinal mucosal damage and development of intestinal inflammation. In this review, the effects of various pro-inflammatory and anti-inflammatory cytokines on intestinal TJ barrier and the progress into the mechanisms that mediate the cytokine modulation of intestinal TJ barrier are reviewed.
引用
收藏
页码:2765 / 2778
页数:14
相关论文
共 126 条
[81]   Inhibition of oxidant-induced barrier disruption and protein tyrosine phosphorylation in Caco-2 cell monolayers by epidermal growth factor [J].
Rao, R ;
Baker, RD ;
Baker, SS .
BIOCHEMICAL PHARMACOLOGY, 1999, 57 (06) :685-695
[82]   PROINFLAMMATORY CYTOKINES IN INTESTINAL-MUCOSA [J].
REINECKER, HC ;
STEFFEN, M ;
DOEHN, C ;
PETERSEN, J ;
PFLUGER, I ;
VOSS, A ;
RAEDLER, A .
IMMUNOLOGIC RESEARCH, 1991, 10 (3-4) :247-248
[83]   Transforming growth factor β1 ameliorates intestinal epithelial barrier disruption by Cryptosporidium parvum in vitro in the absence of mucosal T lymphocytes [J].
Roche, JK ;
Martins, CAP ;
Cosme, R ;
Fayer, R ;
Guerrant, RL .
INFECTION AND IMMUNITY, 2000, 68 (10) :5635-5644
[84]   Systemic bacteraemia following haemorrhagic shock in mice: Alleviation with oral interleukin 6 [J].
Rollwagen, FM ;
Li, YY ;
Pacheco, ND ;
Nielsen, TB .
CYTOKINE, 1996, 8 (02) :121-129
[85]   Microvascular effects of oral interleukin-6 on ischemia/reperfusion in the murine small intestine [J].
Rollwagen, FM ;
Li, YY ;
Pacheco, ND ;
Dick, EJ ;
Kang, YH .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 156 (04) :1177-1182
[86]  
ROY PM, 2006, GASTROENTEROLOGY
[87]   EFFECTS OF MALIGNANCY AND INTERLEUKIN-2 INFUSION ON GUT MACROMOLECULAR PERMEABILITY [J].
RYAN, CM ;
ATKINS, MB ;
MIER, JW ;
GELFAND, JA ;
TOMPKINS, RG .
CRITICAL CARE MEDICINE, 1995, 23 (11) :1801-1806
[88]   The bcl, NFκB and p53/p21WAF1 systems are involved in spontaneous apoptosis and in the anti-apoptotic effect of TGF-β or TNF-α on activated hepatic stellate cells [J].
Saile, B ;
Matthes, N ;
El Armouche, H ;
Neubauer, K ;
Ramadori, G .
EUROPEAN JOURNAL OF CELL BIOLOGY, 2001, 80 (08) :554-561
[89]  
Sanders SE, 1995, EPITHELIAL CELL BIOL, V4, P25
[90]  
Schmitz H, 1999, J CELL SCI, V112, P137