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Intestinal inflammation and barrier function in HLA-B27/beta 2-microglobulin transgenic rats
P D Lundin1, G Ekström, M Erlansson
1Dept. of Animal Physiology, Lund University, Sweden.
Scandinavian Journal of Gastroenterology
|July 1, 1997
Summary
In HLA-B27 transgenic rats, intestinal inflammation began before barrier function was impaired. This suggests inflammation is the initial event in this model, not a consequence of a leaky gut.
Area of Science:
- Gastroenterology
- Immunology
- Genetics
Background:
- Intestinal inflammation is linked to compromised barrier function.
- Transgenic rats expressing HLA-B27/human beta 2-microglobulin spontaneously develop intestinal inflammation.
- This model allows investigation into the sequence of inflammation and barrier dysfunction.
Purpose of the Study:
- To determine whether intestinal inflammation or impaired barrier function occurs first in HLA-B27 transgenic rats.
- To elucidate the etiological sequence in spontaneous intestinal inflammation.
Main Methods:
- Transgenic and control rats (9-14 weeks old) were administered marker molecules (51Cr-EDTA, DDAVP, albumin).
- Marker levels were quantified in blood and urine to assess intestinal permeability.
- Histology and myeloperoxidase content were used to confirm intestinal inflammation.
Main Results:
- Early signs of inflammation (reduced weight gain, urine output, diarrhea) appeared at 12 weeks.
- All transgenic rats showed confirmed intestinal inflammation by 14-15 weeks.
- No significant difference in intestinal marker passage was observed between transgenic and control rats during the study period.
Conclusions:
- Intestinal inflammation precedes the onset of altered intestinal barrier function in this HLA-B27 rat model.
- Inflammation is the initiating event, rather than a consequence of barrier defects.