CD4+ T cells mediate superantigen-induced abnormalities in murine jejunal ion transport

被引:34
作者
McKay, DM [1 ]
Benjamin, MA [1 ]
Lu, J [1 ]
机构
[1] McMaster Univ, Intestinal Dis Res Program, Dept Pathol, Hamilton, ON L8N 3Z5, Canada
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 1998年 / 275卷 / 01期
关键词
Staphylococcus aureus enterotoxin B; intestine;
D O I
10.1152/ajpgi.1998.275.1.G29
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
The immunomodulatory properties of bacterial superantigens (SAgs) have been defined, yet comparatively little is known of how SAgs may affect enteric physiology. Staphylococcus aureus enterotoxin B (SEB) was used to examine the ability of SAgs to alter epithelial ion transport. BALB/c mice, severe combined immunodeficient (SCID, lack T cells) mice, or SCID mice reconstituted with lymphocytes or CD4(+) T cells received SEB intraperitoneally, and jejunal segments were examined in Ussing chambers; controls received saline only. Baseline short-circuit current (I-sc, indicates net ion transport) and I-sc responses evoked by electrical nerve stimulation, histamine, carbachol, or forskolin were recorded. Serum levels of interleukin-fl (IL-2) and interferon-gamma (IFN-gamma) were measured. SEB-treated BALB/c mice showed elevated serum IL-2 and IFN-gamma levels, and jejunal segments displayed a time-and dose-dependent increase in baseline I-sc compared with controls. Conversely, evoked ion secretion was selectively reduced in jejunum from SEB-treated mice. Elevated cytokine levels and changes in jejunal I-sc were not observed in SEB-treated SCID mice. In contrast, SCID mice reconstituted with T cells were responsive to SEB challenge as shown by increased cytokine production and altered jejunal I-sc responses that were similar to those observed in jejunum from SEB-treated BALB/c mice. We conclude that exposure to a model bacterial SAg causes distinct changes in epithelial physiology and that these events can be mediated by CD4(+) T cells.
引用
收藏
页码:G29 / G38
页数:10
相关论文
共 48 条
[1]   THE BIOLOGY OF THE SCID MUTATION [J].
ANSELL, JD ;
BANCROFT, GJ .
IMMUNOLOGY TODAY, 1989, 10 (10) :322-325
[2]  
BARRETT KE, 1993, AM J PHYSIOL, V265, pC859
[3]  
BARRETT KE, 1991, TXB GASTROENTEROLOGY, P265
[4]   EFFECTS OF STAPHYLOCOCCAL ENTEROTOXIN-A ON THE RAT GASTROINTESTINAL-TRACT [J].
BEERY, JT ;
TAYLOR, SL ;
SCHLUNZ, LR ;
FREED, RC ;
BERGDOLL, MS .
INFECTION AND IMMUNITY, 1984, 44 (02) :234-240
[5]   DISRUPTION OF COLONIC ELECTROLYTE TRANSPORT IN EXPERIMENTAL COLITIS [J].
BELL, CJ ;
GALL, DG ;
WALLACE, JL .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1995, 268 (04) :G622-G630
[6]   Changes in murine jejunal morphology evoked by the bacterial superantigen Staphylococcus aureus enterotoxin B are mediated by CD4+ T cells [J].
Benjamin, MA ;
Lu, J ;
Donnelly, G ;
Dureja, P ;
McKay, DM .
INFECTION AND IMMUNITY, 1998, 66 (05) :2193-2199
[7]   DISTRIBUTION AND KINETICS OF SUPERANTIGEN-INDUCED CYTOKINE GENE-EXPRESSION IN MOUSE SPLEEN [J].
BETTE, M ;
SCHAFER, MKH ;
VANROOIJEN, N ;
WEIHE, E ;
FLEISCHER, B .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (05) :1531-1540
[8]   Inflammatory bowel disease: An immunity-mediated condition triggered by bacterial infection with Helicobacter hepaticus [J].
Cahill, RJ ;
Foltz, CJ ;
Fox, JG ;
Dangler, CA ;
Powrie, F ;
Schauer, DB .
INFECTION AND IMMUNITY, 1997, 65 (08) :3126-3131
[9]   EVIDENCE FOR SUPERANTIGEN INVOLVEMENT IN INSULIN-DEPENDENT DIABETES-MELLITUS ETIOLOGY [J].
CONRAD, B ;
WEIDMANN, E ;
TRUCCO, G ;
RUDERT, WA ;
BEHBOO, R ;
RICORDI, C ;
RODRIQUEZRILO, H ;
FINEGOLD, D ;
TRUCCO, M .
NATURE, 1994, 371 (6495) :351-355
[10]   T helper cell 1-type CD4(+) T cells, but not B cells, mediate colitis in interleukin 10-deficient mice [J].
Davidson, NJ ;
Leach, MW ;
Fort, MM ;
ThompsonSnipes, L ;
Kuhn, R ;
Muller, W ;
Berg, DJ ;
Rennick, DM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (01) :241-251