| First Author | Blum AM | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 10 | Pages | 6080-5 |
| PubMed ID | 10229849 | Mgi Jnum | J:90864 |
| Mgi Id | MGI:3044882 | Doi | 10.4049/jimmunol.162.10.6080 |
| Citation | Blum AM, et al. (1999) The substance P receptor is necessary for a normal granulomatous response in murine schistosomiasis mansoni. J Immunol 162(10):6080-5 |
| abstractText | Immune cells within the granulomas of murine schistosomiasis mansoni make the neuropeptide substance P (SP) and express neurokine 1 receptor, which is the specific receptor for substance P (SPr). It was determined if mice with deletion of the SPr (SPr-/-) would develop a normal granulomatous response to schistosome ova during the course of natural infection. Mean liver granuloma size was smaller in SPr-/- mice compared with that of wild-type control animals. Although flow analysis revealed little difference in the cellular composition of the granulomas, both splenocytes and granuloma cells from SPr-/- mice produced much less IFN-gamma and IgG2a and less IgE. The expression of Th2 cytokines (IL-4/IL-5) and IgG1 was comparable to the wild-type control. The mouse with targeted disruption of its SPr had the nonmammalian gene encoding the enzyme beta-galactosidase inserted in exon 1 of the SPr gene. There was beta-galactosidase activity in many mononuclear cells scattered throughout the schistosome granulomas of SPr-/- mice. Also, a granuloma T cell line derived from this transgenic mouse produced beta-galactosidase. These results provide further evidence that in murine schistosomiasis SPr is displayed commonly on granuloma inflammatory cells and is important for granuloma development and expression of IFN-gamma circuitry in this natural infection. |
