Open AccessIntravenous immunoglobulin (IVIG) treatment of experimental colitis induced by dextran sulfate sodium in rats
Author(s) -
SHINTANI N.,
NAKAJIMA T.,
NAKAKUBO H.,
NAGAI H.,
KAGITANI Y.,
TAKIZAWA H.,
ASAKURA H.
Publication year - 1997
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1997.d01-1021.x
Subject(s) - ulcerative colitis , colitis , immunology , proinflammatory cytokine , tumor necrosis factor alpha , peripheral blood mononuclear cell , antibody , medicine , lamina propria , pathology , in vitro , inflammation , chemistry , epithelium , biochemistry , disease
We investigated the therapeutic effect and immunological action mechanism of IgG in experimental colitis induced by 3% dextran sulfate sodium in rats. Intravenous injection of homologous (rat) IgG (400 mg/kg per day) caused a significant suppression of occult blood discharge and ulcerative lesions in the colon, while no suppressive effect was observed in the case of heterologous (human) IgG. The positive effect of rat IgG on the lesions was also clearly shown by the histological examinations. Generation of proinflammatory cytokines, i.e. tumour necrosis factor‐alpha (TNF‐α) and IL‐1α, in the lesions was found to be inhibited by administration of rat IgG. Little or no suppressive action was exerted by human IgG. Careful examination of recruited T cells and macrophages, both of which are thought to play important roles in the development of ulcerative colitis, indicated that rat IgG, but not its human counterpart, decreased the number of immunocompetent cells in colonic mucosa. Meanwhile, in an in vitro study, both forms of IgG were shown to suppress production of TNF‐α and IL‐1α from lamina propria mononuclear cells isolated from rat colon. These findings suggest that, mainly by suppressing recruitment of immunocompetent cells into the lesions, homologous IgG may reduce the occurrence of colitis.