| Autor: |
Öhman, L., Willén, R., Hultgren, O. H., Hultgren Hörnquist, E. |
| Předmět: |
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| Zdroj: |
Clinical & Experimental Immunology; Jul2005, Vol. 141 Issue 1, p37-46, 10p |
| Abstrakt: |
Mice deficient for the inhibitory G protein subunit α2 (G αi2–/–) spontaneously develop a progressive inflammatory bowel disease resembling ulcerative colitis, and have a T helper 1 (Th1)-dominated immune response prior to onset of colitis, which is further augmented after the onset of disease. The present study was performed to investigate whether the G αi2–/– mice were able to down-regulate the Th1-dominated inflammatory mucosal immune response and/or induce an anti-inflammatory Th2/T regulatory response and thereby diminish the severity of colitis following treatment with acellular Bordetella pertussis vaccine . The acellular vaccine against B. pertussis, the causative agent of whooping cough, has been demonstrated to induce a Th2-mediated response in both man and mice. We therefore treated Gαi2–/– mice intraperitoneally with a three-component acellular B. pertussis vaccine. The treated Gαi2–/– mice showed significantly increased interleukin (IL)-10 production in intestinal tissue, associated with significantly reduced colitis and decreased mortality, compared to untreated Gαi2–/– mice. The attenuation of colitis in Gαi2–/– mice was due, at least partly, to the B. pertussis surface antigen filamentous haemagglutinin (FHA), which almost completely inhibited proliferation of CD4+ T cells and stimulated apoptosis of activated CD4+ T helper 1 cells. In conclusion, the three-component acellular B. pertussis vaccine containing filamentous haemagglutinin increases the production of IL-10 in the intestinal mucosa, induces apoptosis of activated Th1 cells and attenuates colitis in Gαi2–/– mice. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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