The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation
Abstract
Exposure to dextran sulfate sodium (DSS) induces acute colitis, which is normally resolved after DSS removal. To study chronicity, mice are typically subjected to three to five cycles of weekly DSS exposures, each followed by a 1- to 2-wk rest period. Here, we describe a novel and convenient way of inducing chronic, progressive colitis by a single exposure to DSS. C57BL/6 mice exposed to DSS for 5 days developed acute colitis that progressed to severe chronic inflammation. The plasma haptoglobin levels remained high during the chronic phase, showing that the inflammation was active. Surprisingly, the mice regained their original weight along with the progression of colitis, and the only apparent symptom was loose feces. Histopathological changes 4 wk after DSS removal were dense infiltrates of mononuclear cells, irregular epithelial structure, and persistent deposits of collagen. A progressive production of the cytokines IL-1β, IL-12 p70, and IL-17 correlated with the extensive cellular infiltration, whereas high IFN-γ production was mainly found late in the chronic phase. Similar to C57BL/6 mice, BALB/c mice exposed to 5 days of DSS developed acute colitis as previously described. The acute colitis was accompanied by elevated plasma levels of haptoglobin and increased colonic levels of IL-1α/β, IL-6, IL-18, and granulocyte colony-stimulating factor. However, soon after DSS removal, BALB/c mice recovered and were symptom free within 2 wk and completely recovered 4 wk after DSS removal in terms of histopathology, haptoglobin levels, and local cytokine production. In summary, these data stress the effect of genetic background on the outcome of DSS provocation. We believe that the present protocol to induce chronic colitis in C57BL/6 mice offers a robust model for validating future therapies for treatment of inflammatory bowel disease.
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Cited by
Regulation of inflammatory responses by IL-17F
Yang, X. O., Chang, S. H., Park, H., Nurieva, R., Shah, B., Acero, L., Wang, Y.-H., Schluns, K. S., Broaddus, R. R., Zhu, Z., et al. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20071978 · Cited by 739
Kang, C.-S., Ban, M., Choi, E.-J., Moon, H.-G., Jeon, J.-S., Kim, D.-K., Park, S.-K., Jeon, S. G., Roh, T.-Y., Myung, S.-J., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0076520 · Cited by 543
Chitin nanofibers: preparations, modifications, and applications
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The Hydroxylase Inhibitor Dimethyloxalylglycine Is Protective in a Murine Model of Colitis
Cummins, E. P., Seeballuck, F., Keely, S. J., Mangan, N. E., Callanan, J. J., Fallon, P. G., & Taylor, C. T. (2008) · Gastroenterology · doi:10.1053/j.gastro.2007.10.012 · Cited by 407
Metadata
- Authors
- Melgar, S., Karlsson, A., & Michaëlsson, E.
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2005-06
- Volume
- 288
- Issue
- 6
- Pages
- G1328-G1338
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W2149958822
- Cited by
- 578
- References
- 53
- FWCI
- 9.24
- Type
- journal article
- Language
- en
- Open access
- closed
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- Melgar, S., Karlsson, A., & Michaëlsson, E. (2005). Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. American Journal of Physiology-Gastrointestinal and Liver Physiology. https://doi.org/10.1152/ajpgi.00467.2004
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