AJP - GI Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 291: G1155-G1162, 2006. First published August 10, 2006; doi:10.1152/ajpgi.00446.2005
0193-1857/06 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
291/6/G1155    most recent
00446.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Angulo, S.
Right arrow Articles by Panés, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Angulo, S.
Right arrow Articles by Panés, J.

INFLAMMATION/IMMUNITY/MEDIATORS

Lactobacillus casei prevents the upregulation of ICAM-1 expression and leukocyte recruitment in experimental colitis

Sandra Angulo,1 Marta Llopis,2 María Antolín,2 Meritxell Gironella,1 Miquel Sans,1 Juan Ramon Malagelada,2 Josep Maria Piqué,1 Francisco Guarner,2 and Julián Panés1

1Department of Gastroenterology, Hospital Clínic of Barcelona, University of Barcelona; and 2Digestive System Research Unit, University Hospital Vall d'Hebron, Barcelona, Spain

Submitted 20 September 2005 ; accepted in final form 13 July 2006

Lactobacillus casei has been shown to attenuate the severity of experimental colitis. The objective of the present study was to determine whether the effects of L. casei on colitis are related to modulation of leukocyte recruitment into the inflamed intestine. Rats with a colonic segment excluded from fecal transit were surgically prepared. The segment was decontaminated with antibiotics and recolonized with normal flora isolated from the inflamed rat colon, associated or not to L. casei. Control and colitic [2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced] animals were studied. Leukocyte-endothelial cell interactions were characterized in the colonic microcirculation by intravital microscopy, and ICAM-1 and VCAM-1 expression was measured by the radiolabeled antibody technique. Compared with the noninflamed colonic segment, induction of colitis by TNBS provoked a marked increase in the number of leukocytes firmly adherent to the venular wall (0.5 ± 0.1 vs. 2.1 ± 0.6 leukocytes/100 µm, P < 0.01). Colonization with L. casei significantly reduced the number of adherent leukocytes (1.3 ± 0.4 leukocytes/100 µm; P < 0.05) but did not affect the increased rolling interactions associated with the induction of colitis. Compared with the noncolitic group, induction of colitis was associated with a marked increase in ICAM-1 expression (117 ± 4 vs. 180 ± 3 ng antibody/g tissue) that was abrogated when the colitic segment was colonized by L. casei (117 ± 3 ng antibody/g tissue, P < 0.05). However, L. casei administration did not modify VCAM-1 upregulation in colitic animals. L. casei attenuates leukocyte recruitment observed in experimental colitis induced by TNBS. This effect is possibly related to abrogation of ICAM-1 upregulation.

inflammatory bowel diseases; probiotics; cell adhesion molecules; endothelium


Address for reprint requests and other correspondence: J. Panes, Dept. of Gastroenterology, Hospital Clínic, Villarroel 170, Barcelona 08036, Spain (e-mail: panes{at}ub.edu)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.