Bacterial load in animal models of acute and chronic 'reactivated' colitis

被引:22
作者
Hernández, GA [1 ]
Appleyard, CB [1 ]
机构
[1] Ponce Sch Med, Dept Physiol, Ponce, PR 00732 USA
关键词
bacteria; colitis; rat model; dextran sulfate sodium; trinitrobenzene sulfonic acid;
D O I
10.1159/000071296
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background. The involvement of enteropathogenic microorganisms in the pathogenesis of inflammatory bowel disease (IBD) and their importance in the different phases of inflammation are still unknown. Aim:To quantify the aerobic bacterial load in models of acute and chronic 'reactivated' colitis, and correlate this with damage. Methods: Acute colitis was induced in rats by administration of trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS). Colitis was 'reactivated' 6 weeks later by intravenous administration of TNBS. The distal colon was removed and scored macroscopically before inoculating samples. Results: Bacterial load in rats with acute colitis (72 h) and chronic 'reactivated' colitis or their controls was significantly higher than untreated (p < 0.05); however, there were significantly more bacteria in acute colitis than in chronic 'reactivated' or their controls (p < 0.05). Both acute and chronic 'reactivated' colitis had significantly higher damage scores than untreated animals (p < 0.05). Bacterial load and damage score were significantly correlated only with acute colitis. Conclusions: The role of enteric microflora in the pathogenesis of IBD is greater during the acute phase of colitis. The correlation between bacterial load and tissue damage suggests that damage contributes to bacterial multiplication and exacerbation of colitis. Normal colonic flora may contribute to the relapse of the disease. Copyright © 2003 S. Karger AG, Basel.
引用
收藏
页码:161 / 169
页数:9
相关论文
共 23 条
[1]   REACTIVATION OF HAPTEN-INDUCED COLITIS AND ITS PREVENTION BY ANTIINFLAMMATORY DRUGS [J].
APPLEYARD, CB ;
WALLACE, JL .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1995, 269 (01) :G119-G125
[2]   Persistent epithelial dysfunction and bacterial translocation after resolution of intestinal inflammation [J].
Asfaha, S ;
MacNaughton, WK ;
Appleyard, CB ;
Chadee, K ;
Wallace, JL .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2001, 281 (03) :G635-G644
[3]   MEASUREMENT OF CUTANEOUS INFLAMMATION - ESTIMATION OF NEUTROPHIL CONTENT WITH AN ENZYME MARKER [J].
BRADLEY, PP ;
PRIEBAT, DA ;
CHRISTENSEN, RD ;
ROTHSTEIN, G .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1982, 78 (03) :206-209
[4]  
Colombel JF, 1997, GASTROENTEROLOGY, V112, pA951
[5]   The Crohn's disease-associated bacterial protein I2 is a novel enteric T cell superantigen [J].
Dalwadi, H ;
Wei, B ;
Kronenberg, M ;
Sutton, CL ;
Braun, J .
IMMUNITY, 2001, 15 (01) :149-158
[6]  
*DIFC LAB, 1984, DEH CULT MED REAG MI, P140
[7]   EXPERIMENTAL-MODELS OF INFLAMMATORY BOWEL-DISEASE [J].
ELSON, CO ;
SARTOR, RB ;
TENNYSON, GS ;
RIDDELL, RH .
GASTROENTEROLOGY, 1995, 109 (04) :1344-1367
[8]   Incrimination of anaerobic bacteria in the induction of experimental colitis [J].
GarciaLafuente, A ;
Antolin, M ;
Guarner, F ;
Crespo, E ;
Salas, A ;
Forcada, P ;
Laguarda, M ;
Gavalda, J ;
Baena, JA ;
Vilaseca, J ;
Malagelada, JR .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1997, 272 (01) :G10-G15
[9]   The role of the resident intestinal flora in acute and chronic dextran sulfate sodium-induced colitis in mice [J].
Hans, W ;
Schölmerich, J ;
Gross, V ;
Falk, W .
EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY, 2000, 12 (03) :267-273
[10]  
Hata K, 2001, SCAND J GASTROENTERO, V36, P1185