CICLOSPORIN-DEPENDENT, NU-INDEPENDENT, MUCOSAL INTERLEUKIN-6 RESPONSE TO GRAM-NEGATIVE BACTERIA

被引:12
作者
HEDGES, S
LINDER, H
DEMAN, P
EDEN, CS
机构
[1] Department of Clinical Immunology, University of Göteborg
关键词
D O I
10.1111/j.1365-3083.1990.tb02776.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
Regulation of the mucosal inflammatory response to Gram‐negative bacteria was analysed. The interleukin 6 (IL‐6) secretion, influx of polymorphonuclear leucocytes into urine, and bacterial clearance from the kidneys were compared between Balb/c (nu/nu) and nu/± mice, with and without ciclosporin (CsA) treatment. There was no significant influence of the nu genotype on any of the host responses measured. CsA pretreatment significantly decreased II‐6 secretion in both nu/nu and nu/± mice, but did not affect bacterial clearance or the leucocyte response in any mouse strain tested. Tissue damage, in addition to bacterial infection, resulted in significantly higher levels of IL‐6 than bacterial infection alone. Tissue‐damaged mice were significantly less likely to clear the bacterial infection than their non‐damaged counterparts, but there was no significant difference in the leucocyte response. CsA pretreatment did not significantly reduce the levels of IL‐6 in the tissue‐damaged mice. These results demonstrate that the mucosal inflammatory response to Gram‐negative infection, including IL‐6 secretion, is nu‐independent, and that bacterial infection alone or in combination with tissue damage induce IL‐6 secretion by two different pathways. Copyright © 1990, Wiley Blackwell. All rights reserved
引用
收藏
页码:335 / 343
页数:9
相关论文
共 33 条
[1]   PRODUCTION OF HYBRIDOMA GROWTH-FACTOR BY HUMAN-MONOCYTES [J].
AARDEN, LA ;
DEGROOT, ER ;
SCHAAP, OL ;
LANSDORP, PM .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1987, 17 (10) :1411-1416
[2]  
BEAGLEY KW, 1989, INT C MUCOSAL IMMUNO
[3]  
BEUTLER BA, 1985, J IMMUNOL, V135, P3972
[4]   CYCLOSPORIN-A MEDIATES IMMUNOSUPPRESSION OF PRIMARY CYTO-TOXIC T-CELL RESPONSES BY IMPAIRING THE RELEASE OF INTERLEUKIN-1 AND INTERLEUKIN-2 [J].
BUNJES, D ;
HARDT, C ;
ROLLINGHOFF, M ;
WAGNER, H .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1981, 11 (08) :657-661
[5]   INTERLEUKIN-6 INDUCED AT MUCOSAL SURFACES BY GRAM-NEGATIVE BACTERIAL-INFECTION [J].
DEMAN, P ;
VANKOOTEN, C ;
AARDEN, L ;
ENGBERG, I ;
LINDER, H ;
EDEN, CS .
INFECTION AND IMMUNITY, 1989, 57 (11) :3383-3388
[6]   GENETIC-FACTORS IN HOST-RESISTANCE TO URINARY-TRACT INFECTION [J].
EDEN, CS ;
BRILES, D ;
HAGBERG, L ;
MCGHEE, J ;
MICHALEC, S .
INFECTION, 1984, 12 (02) :118-123
[7]  
EDEN CS, 1988, J IMMUNOL, V140, P3180
[8]  
FUJIHASHI K, 1989, INT C MUCOSAL IMMUNO
[9]   INTERFERON BETA-2/B-CELL STIMULATORY FACTOR TYPE-2 SHARES IDENTITY WITH MONOCYTE-DERIVED HEPATOCYTE-STIMULATING FACTOR AND REGULATES THE MAJOR ACUTE PHASE PROTEIN RESPONSE IN LIVER-CELLS [J].
GAULDIE, J ;
RICHARDS, C ;
HARNISH, D ;
LANSDORP, P ;
BAUMANN, H .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (20) :7251-7255
[10]  
GRANELLIPIPERNO A, 1988, TRANSPLANTATION, V46, pS53