N. Shintani et al., INTRAVENOUS IMMUNOGLOBULIN (IVIG) TREATMENT OF EXPERIMENTAL COLITIS INDUCED BY DEXTRAN SULFATE SODIUM IN RATS, Clinical and experimental immunology, 108(2), 1997, pp. 340-345
We investigated the therapeutic effect and immunological action mechan
ism of IgG in experimental colitis induced by 3% dextran sulfate sodiu
m in rats. Intravenous injection of homologous (rat) IgG (400 mg/kg pe
r day) caused a significant suppression of occult blood discharge and
ulcerative lesions in the colon, while no suppressive effect was obser
ved in the case of heterologous (human) IgG. The positive effect of ra
t IgG on the lesions was also clearly shown by the histological examin
ations. Generation of proinflammatory cytokines, i.e. tumour necrosis
factor-alpha (TNF-alpha) and IL-1 alpha, in the lesions was found to b
e inhibited by administration of rat IgG. Little or no suppressive act
ion 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 no
t 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-alpha and IL-1 alpha from la
mina propria mononuclear cells isolated from rat colon. These findings
suggest that, mainly by suppressing recruitment of immunocompetent ce
lls into the lesions, homologous IgG may reduce the occurrence of coli
tis.