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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Ruminant Diseases and Immunology Research » Research » Publications at this Location » Publication #117891
Title: SUBSTANCE P-BINDING SITES ARE INCREASED IN T-CELL RECEPTOR ALPHA-DEFICIENT (TCRA-) MICE WITH INFLAMMATORY BOWEL DISEASE (IBD)

Author
item SONEA, I - IOWA STATE UNIV., AMES
item WANNEMUEHLER, M - IOWA STATE UNIV., AMES
item WEINSTOCK, J - UNIV. IA, IOWA CITY, IA
item Waters, Wade
item ELLIOTT, D - UNIV. IA, IOWA CITY, IA
item Harp, James

Submitted to: Society for Neuroscience Abstracts and Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 10/24/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: To determine whether TCRa- mice provide a suitable tool to study neuroimmune interactions in IBD, we sought to determine whether substance P binding sites were upregulated in TCRa- mice with IBD, as they are in humans with IBD. Using autoradiography, we demonstrated that substance P binding sites were upregulated in the lamina propria of TCRa- mice with IBD, when compared to unaffected TCRa- mice, or immunocompetent C57B16/J mice. These binding sites corresponded to an authentic neurokinin receptor, since nonspecific binding was eliminated in the presence of an excess of nonradioactive substance P, greatly decreased in the presence of substance P (4-11), but not by substance P (1-4). The neurokinin- I receptor was detected using immunohistochemistry in both healthy and IBD- affected intestine in TCRa- mice: it was present in myenteric and submyenteric intestinal neurons, on enteric smooth muscle, and on cells within the lamina propria and lymphoid aggregates. The extent and intensity of neurokinin- 1 receptor immunoreactivity was greatly enhanced in IBD-affected TCRa- mice, compared to unaffected TCRa- or C57BL6/J mice. Substance P receptors are thus upregulated in IBD-affected TCRa- mice, as they are in patients with IBD, and will provide a valuable tool to investigate neuroimmune interactions in the inflamed gut.