Mast cell deficient W/W^V mice lack stress-induced increase in serum IL-6 levels, as well as in peripheral CRH and vascular permeability, a model of rheumatoid arthritis

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/W^V mast 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/W^V mast cell deficient mice. Vascular permeability to ⁹⁹Tc, as well as local CRH levels, were also increased by stress, but not in W/W^V mice. 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.