Background: A/JCr mice develop typhlitis in response to Helicobacter hepaticus infection, whereas C57BL/6 mice coexist with this bacterium in a "commensal" relationship and do not develop disease even during prolonged colonization. ## Methods: To determine mechanisms that control this balance bet
Serum biomarkers in a mouse model of bacterial-induced inflammatory bowel disease
โ Scribed by Anne E. Torrence; Thea Brabb; Joanne L. Viney; Helle Bielefeldt-Ohmann; Piper Treuting; Audrey Seamons; Rolf Drivdahl; Weiping Zeng; Lillian Maggio-Price
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 206 KB
- Volume
- 14
- Category
- Article
- ISSN
- 1078-0998
No coin nor oath required. For personal study only.
โฆ Synopsis
Background:
The diagnosis and classification of inflammatory bowel disease (IBD) require both clinical and histopathologic data. Serum biomarkers would be of considerable benefit to noninvasively monitor the progression of disease, assess effectiveness of therapies, and assist in understanding disease pathogenesis. Currently, there are limited noninvasive biomarkers for monitoring disease progression in animal IBD models, which are used extensively to develop new therapies and to understand IBD pathogenesis.
Methods: Serum biomarkers of early and late IBD were identified using multianalyte profiling in mdr1a ฯช/ฯช mice with IBD triggered by infection with Helicobacter bilis. The correlation of changes in these biomarkers with histopathology scores and clinical signs in the presence and in the absence of antibiotic treatment was determined.
Results: Serum levels of interleukin (IL)-11, IL-17, 10-kDa interferon-โฅ-inducible protein (IP-10), lymphotactin, monocyte chemoattractant protein (MCP)-1, and vascular cell adhesion molecule (VCAM)-1 were elevated early in IBD. In late, more severe IBD, serum levels of IL-11, IP-10, haptoglobin, matrix metalloproteinase-9, macrophage inflammatory protein (MIP)-1โฅ, fibrinogen, immunoglobulin A, MIP-3 beta (โค), VCAM-1, apolipoprotein (Apo) A1, and IL-18 were elevated. All late serum biomarkers except Apo A1 correlated with histopathology scores. Antibiotic treatment improved clinical signs of IBD and decreased mean serum values of many of the biomarkers. For all biomarkers, the individual pathol-ogy scores correlated significantly with individual serum analyte levels after treatment.
Conclusions:
Serum analyte measurement is a useful, noninvasive method for monitoring disease in a mouse model of bacterialinduced IBD.
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