The role of epithelial Toll-like receptor expression in host defense and microbial tolerance

被引:49
作者
Hornef, MW
Bogdan, C
机构
[1] Univ Clin Freiburg, Dept Med Microbiol, Inst Med Microbiol & Hyg, D-79104 Freiburg, Germany
[2] Swedish Inst Infect Dis Control SMI, Stockholm, Sweden
来源
JOURNAL OF ENDOTOXIN RESEARCH | 2005年 / 11卷 / 02期
关键词
epithelial cells; TLR expression; host defense; microbial tolerance;
D O I
10.1179/096805105X35224
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
The recognition of microbial structures by Toll-like receptors (TLRs) on professional immune cells situated at sterile internal body sites occurs during invasive microbial infection. It indicates infectious non-self and thereby represents the adequate co-stimulatory signal to initiate activation of the adaptive immune system against the invading pathogen. In contrast, most epithelial body surfaces are permanently colonized by microbial organisms of the normal flora and thus TLR ligands are present under physiological conditions. In the following, we discuss the characteristics of TLR-mediated recognition by epithelial cells, the subsequent activation of the host immune system, and protective mechanisms that might help to avoid inadequate stimulation and allow differentiation between commensal or pathogenic micro-organisms. Recent findings suggest that the role of epithelial cells in the maintenance of stable microbial colonization of host surfaces and the immediate host response to infectious challenges might have to be revised.
引用
收藏
页码:124 / 128
页数:5
相关论文
共 52 条
  • [1] Ahmad-Nejad P, 2002, EUR J IMMUNOL, V32, P1958, DOI 10.1002/1521-4141(200207)32:7<1958::AID-IMMU1958>3.0.CO
  • [2] 2-U
  • [3] Endothelium-derived toll-like receptor-4 is the key molecule in LPS-induced neutrophil sequestration into lungs
    Andonegui, G
    Bonder, CS
    Green, F
    Mullaly, SC
    Zbytnuik, L
    Raharjo, E
    Kubes, P
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (07) : 1011 - 1020
  • [4] Endothelium-derived Toll-like receptor-4 is the key molecule in LPS-induced neutrophil sequestration into lungs (vol. 111, pg. 1011, 2003)
    Andonegui, G
    Bonder, CS
    Green, F
    Mullaly, SC
    Zbytnuik, L
    Raharjo, E
    Kubes, P
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (08) : 1264 - 1264
  • [5] Secretion of microbicidal α-defensins by intestinal Paneth cells in response to bacteria
    Ayabe, T
    Satchell, DP
    Wilson, CL
    Parks, WC
    Selsted, ME
    Ouellette, AJ
    [J]. NATURE IMMUNOLOGY, 2000, 1 (02) : 113 - 118
  • [6] Structural requirements for TLR4-mediated LPS signalling:: a biological role for LPS modifications
    Bäckhed, F
    Normark, S
    Schweda, EKH
    Oscarson, S
    Richter-Dahlfors, A
    [J]. MICROBES AND INFECTION, 2003, 5 (12) : 1057 - 1063
  • [7] Toll-like receptor 4-mediated signaling by epithelial surfaces:: necessity or threat?
    Bäckhed, F
    Hornef, M
    [J]. MICROBES AND INFECTION, 2003, 5 (11) : 951 - 959
  • [8] In vitro and ex vivo activation of the TLR5 signaling pathway in intestinal epithelial cells by a commensal Escherichia coli strain
    Bambou, JC
    Giraud, A
    Menard, S
    Begue, B
    Rakotobe, S
    Heyman, M
    Taddei, FO
    Cerf-Bensussan, N
    Gaboriau-Routhiau, V
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (41) : 42984 - 42992
  • [9] ST2 is an inhibitor of interleukin 1 receptor and Toll-like receptor 4 signaling and maintains endotoxin tolerance
    Brint, EK
    Xu, DM
    Liu, HY
    Dunne, A
    McKenzie, ANJ
    O'Neill, LAJ
    Liew, FY
    [J]. NATURE IMMUNOLOGY, 2004, 5 (04) : 373 - 379
  • [10] Inhibition of interleukin 1 receptor/toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4
    Burns, K
    Janssens, S
    Brissoni, B
    Olivos, N
    Beyaert, R
    Tschopp, J
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (02) : 263 - 268