| Autor: |
Huang, M., Berry, J., Kandere, K., Lytinas, M., Karalis, K., Theoharides, T.C. |
| Zdroj: |
International Journal of Immunopathology and Pharmacology; September 2002, Vol. 15 Issue: 3 p249-254, 6p |
| Abstrakt: |
Corticotropin releasing hormone (CRH) and interleukin-6 (IL-6) are implicated in inflammatory diseases triggered by stress. Acute restraint stress increases serum IL-6 in the blood, but its source is not known. Our current study was carried out in order to determine the contribution of mast cells to stress-induced IL-6 release and to investigate skin CRH and vascular permeability in mice. W/Wvmast cell deficient and their wild type control +/+ mice were stressed in a plexiglass restraint chamber for 60 or 120 min. Serum corticosterone and IL-6 levels were measured. Other mice were injected with 99-Tchnetium gluceptate (99Tc) and its extravastion, indicating vascular permeability, was determined along with CRH levels in the skin and knee joints. Acute stress increased serum IL-6 in mice, but was greatly inhibited in W/Wvmast cell deficient mice. Vascular permeability to 99Tc, as well as local CRH levels, were also increased by stress, but not in W/Wvmice. Findings from our current study suggest a link between mast cells and stress-related skin and joint inflammation and may explain initial events in psoriatic and rheumatoid arthritis. |
| Databáze: |
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