Minireview: Functions of the renal tract epithelium in coordinating the innate immune response to infection

被引:43
作者
Chowdhury, P [1 ]
Sacks, SH [1 ]
Sheerin, NS [1 ]
机构
[1] Univ London Kings Coll, Guys Hosp, Dept Nephrol & Transplantat, London SE1 9RT, England
基金
英国惠康基金;
关键词
renal epithelial cells; urinary tract infection; toll-like receptors; complement; interleukin-8; defensins;
D O I
10.1111/j.1523-1755.2004.00896.x
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Infection of the urinary tract remains one of the most common infections affecting mankind. Renal epithelial cells, being one of the first cells to come into contact with invading organisms, are in a key position to coordinate host defense. The epithelium not only provides a physical barrier to infection, but can also augment the immune response via the production of a number of inflammatory mediators and antimicrobial proteins. Recent work has demonstrated that cells of the innate immune system, including epithelial cells, express toll-like receptors (TLRs), with the capacity to recognize bacterial components. Although the exact mechanisms remain unclear, engagement of TLRs can lead to epithelial cell activation and the production of inflammatory mediators. These include complement proteins, other bactericidal peptides, and chemotactic cytokines. The resulting inflammatory infiltrate serves to aid bacterial clearance, but can also lead to renal damage. In this review, we describe how renal epithelial cells contribute to the innate immune response to ascending urinary tract infection. We specifically relate previous work to more recent developments in this field. An improved understanding of the mechanisms involved may highlight potential therapeutic avenues to aid bacterial clearance and prevent the renal scarring associated with infection.
引用
收藏
页码:1334 / 1344
页数:11
相关论文
共 120 条
[1]   Lipopolysaccharide interaction with cell surface toll-like receptor 4-MD-2: Higher affinity than that with MD-2 or CD14 [J].
Akashi, S ;
Saitoh, S ;
Wakabayashi, Y ;
Kikuchi, T ;
Takamura, N ;
Nagai, Y ;
Kusumoto, Y ;
Fukase, K ;
Kusumoto, S ;
Adachi, Y ;
Kosugi, A ;
Miyake, K .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (07) :1035-1042
[2]   Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].
Alexopoulou, L ;
Holt, AC ;
Medzhitov, R ;
Flavell, RA .
NATURE, 2001, 413 (6857) :732-738
[3]   LOCAL TRANSCRIPTION OF COMPLEMENT C3 IN HUMAN ALLOGRAFT REJECTION - EVIDENCE FOR A PATHOGENIC ROLE AND CORRELATION TO HISTOLOGY AND OUTCOME [J].
ANDREWS, PA ;
PANI, A ;
ZHOU, WD ;
SACKS, SH .
TRANSPLANTATION, 1994, 58 (05) :637-640
[4]   Induction of innate immune responses by Escherichia coli and purified lipopolysaccharide correlate with organ- and cell-specific expression of Toll-like receptors within the human urinary tract [J].
Bäckhed, F ;
Söderhäll, M ;
Ekman, P ;
Normark, S ;
Richter-Dahlfors, A .
CELLULAR MICROBIOLOGY, 2001, 3 (03) :153-158
[5]  
BAGGIOLINI M, 1994, ADV IMMUNOL, V55, P97
[6]   Chemokines and leukocyte traffic [J].
Baggiolini, M .
NATURE, 1998, 392 (6676) :565-568
[7]  
BAZIL V, 1991, J IMMUNOL, V147, P1567
[8]   A conserved signaling pathway: The Drosophila Toll-Dorsal pathway [J].
Belvin, MP ;
Anderson, KV .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1996, 12 :393-416
[9]   Toll-like receptor 4-dependent activation of dendritic cells by β-defensin 2 [J].
Biragyn, A ;
Ruffini, PA ;
Leifer, CA ;
Klyushnenkova, E ;
Shakhov, A ;
Chertov, O ;
Shirakawa, AK ;
Farber, JM ;
Segal, DM ;
Oppenheim, JJ ;
Kwak, LW .
SCIENCE, 2002, 298 (5595) :1025-1029
[10]  
BOZIC CR, 1995, J IMMUNOL, V154, P6048