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Importance and regulation of the colonic mucus barrier in a mouse model of colitis.

Artikel i vetenskaplig tidskrift
Författare J Petersson
O Schreiber
Gunnar C. Hansson
S J Gendler
A Velcich
J O Lundberg
S Roos
L Holm
M Phillipson
Publicerad i American journal of physiology. Gastrointestinal and liver physiology
Volym 300
Nummer/häfte 2
Sidor G327-33
ISSN 1522-1547
Publiceringsår 2011
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor G327-33
Språk en
Länkar dx.doi.org/10.1152/ajpgi.00422.2010
Ämnesord Animals, Bacterial Translocation, Colitis, chemically induced, microbiology, pathology, physiopathology, Colon, drug effects, secretion, Dextran Sulfate, Disease Susceptibility, Down-Regulation, Germ-Free Life, Intestinal Mucosa, drug effects, secretion, Lipopolysaccharides, pharmacology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mucin-1, genetics, metabolism, Mucin-2, genetics, metabolism, Peptidoglycan, pharmacology, Severity of Illness Index, T-Lymphocytes, pathology
Ämneskategorier Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)

Sammanfattning

The colonic mucus layer serves as an important barrier and prevents colonic bacteria from invading the mucosa and cause inflammation. The regulation of colonic mucus secretion is poorly understood. The aim of this study was to investigate the role of the mucus barrier in induction of colitis. Furthermore, regulation of mucus secretion by luminal bacterial products was studied. The colon of anesthetized Muc2(-/-), Muc1(-/-), wild-type (wt), and germ-free mice was exteriorized, the mucosal surface was visualized, and mucus thickness was measured with micropipettes. Colitis was induced by DSS (dextran sodium sulfate, 3%, in drinking water), and disease activity index (DAI) was assessed daily. The colonic mucosa of germ-free and conventionally housed mice was exposed to the bacterial products LPS (lipopolysaccharide) and PGN (peptidoglycan). After DSS induction of colitis, the thickness of the firmly adherent mucus layer was significantly thinner after 5 days and onward, which paralleled the increment of DAI. Muc2(-/-) mice, which lacked firmly adherent mucus, were predisposed to colitis, whereas Muc1(-/-) mice were protected with significantly lower DAI by DSS compared with wt mice. The mucus barrier increased in Muc1(-/-) mice in response to DSS, whereas significantly fewer T cells were recruited to the inflamed colon. Mice housed under germ-free conditions had an extremely thin adherent colonic mucus layer, but when exposed to bacterial products (PGN or LPS) the thickness of the adherent mucus layer was quickly restored to levels observed in conventionally housed mice. This study demonstrates a correlation between decreasing mucus barrier and increasing clinical symptoms during onset of colitis. Mice lacking colonic mucus (Muc2(-/-)) were hypersensitive to DSS-induced colitis, whereas Muc1(-/-) were protected, probably through the ability to increase the mucus barrier but also by decreased T cell recruitment to the afflicted site. Furthermore, the ability of bacteria to regulate the thickness of the colonic mucus was demonstrated.

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