Cytokine-mediated control of lipopolysaccharide-induced activation of small intestinal epithelial cells

被引:28
作者
Lotz, Michael
Koenig, Till
Menard, Sandrine
Guetle, Dominique
Bogdan, Christian
Hornef, Mathias W. [1 ]
机构
[1] Univ Clin Freiburg, Inst Med Microbiol & Hyg, Dept Microbiol & Hygiene, Freiburg, Germany
[2] Swedish Inst Infect Disease Control, Stockholm, Sweden
[3] Univ Freiburg, Inst Biol 2, Fac Biol, Freiburg, Germany
关键词
toll-like receptor; mucosal immunology; interleukin; lipopolysaccharide; intestinal mucosa; NITRIC-OXIDE; EXPRESSION; IL-4; STAT6; INTERLEUKIN-4; MECHANISMS; COLITIS; DISEASE;
D O I
10.1111/j.1365-2567.2007.02639.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cytokines with anti-inflammatory properties have been implicated in the prevention of inappropriate immune activation by commensal bacteria in the intestinal tract. Here, we analysed receptor expression, cellular signalling, and the inhibitory activity of interleukin (IL)-4, -10, -11, and -13 as well as of transforming growth factor-beta on lipopolysaccharide-mediated small intestinal epithelial cell activation. Only IL-4 and IL-13 had a significant inhibitory effect on chemokine secretion and nitric oxide (NO) production in differentiated and polarized cells. Reverse transcription-polymerase chain reaction of primary intestinal epithelial cells obtained by laser-microdissection confirmed expression of the type II IL-4 receptor consisting of the IL-4 receptor alpha and the IL-13 receptor alpha 1. Also, IL-4 or IL-13 led to rapid signal transducer and activator of transcription 6 phosphorylation, diminished inducible NO synthase expression, and enhanced the antagonistic arginase 1 activity. In conclusion, cytokines such as IL-4 and IL-13 affect intestinal epithelial cells and exhibit a modulating activity on Toll-like receptor-4-mediated epithelial cell activation.
引用
收藏
页码:306 / 315
页数:10
相关论文
共 19 条
  • [1] Bennett BL, 1997, J BIOL CHEM, V272, P10212
  • [2] IL-4 and IL-13 up-regulate intestinal trefoil factor expression: Requirement for STAT6 and de novo protein synthesis
    Blanchard, C
    Durual, S
    Estienne, M
    Bouzakri, K
    Heim, MH
    Blin, N
    Cuber, JC
    [J]. JOURNAL OF IMMUNOLOGY, 2004, 172 (06) : 3775 - 3783
  • [3] Nitric oxide and the immune response
    Bogdan, C
    [J]. NATURE IMMUNOLOGY, 2001, 2 (10) : 907 - 916
  • [4] Interleukins 4 and 13 increase intestinal epithelial permeability by a phosphatidylinositol 3-kinase pathway - Lack of evidence for STAT 6 involvement
    Ceponis, PJM
    Botelho, F
    Richards, CD
    McKay, DM
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (37) : 29132 - 29137
  • [5] Dabbagh K, 1999, J IMMUNOL, V162, P6233
  • [6] Responses to self and non-self intestinal microflora in health and inflammatory bowel disease
    Duchmann, R
    Neurath, MF
    zum Büschenfelde, KHM
    [J]. RESEARCH IN IMMUNOLOGY, 1997, 148 (8-9): : 589 - 594
  • [7] IL-4 exacerbates disease in a Th1 cell transfer model of colitis
    Fort, MM
    Lesley, R
    Davidson, NJ
    Menon, S
    Brombacher, F
    Leach, MW
    Rennick, DM
    [J]. JOURNAL OF IMMUNOLOGY, 2001, 166 (04) : 2793 - 2800
  • [8] Grunig G., 2003, CYTOKINE HDB, V4th ed., P409, DOI [10.1016/b978-012689663-3/50021-1, DOI 10.1016/B978-012689663-3/50021-1]
  • [9] Interleukin-4 and interleukin-13 signaling connections maps
    Kelly-Welch, AE
    Hanson, EM
    Boothby, MR
    Keegan, AD
    [J]. SCIENCE, 2003, 300 (5625) : 1527 - 1528
  • [10] Translational control of inducible nitric oxide synthase expression by arginine can explain the arginine paradox
    Lee, J
    Ryu, H
    Ferrante, RJ
    Morris, SM
    Ratan, RR
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (08) : 4843 - 4848