Inflammatory bowel disease in scid mice is initiated by transplantation of
CD4(+) T-cells from immunocompetent syngenic donor mice. As the disease pro
gresses, immunoglobulin (Ig)-containing cells appear in the gut lamina prop
ria, suggesting that locally accumulating Ig may play a role in disease dev
elopment. In the present work. we have investigated the relationship betwee
n disease progression and patterns or levels of Ig isotypes in the feces of
scid mice suffering from an ongoing colitis. The data clearly showed that
the severity or progression of the disease did not influence the levels of
IgA, IgG1, IgG2a, IgG2b, and IgG3, whereas the level of fecal IgM increased
during the course of colitis. The presence of the serum protein alpha-1-an
titrypsin in fecal extracts from diseased mice suggests that some of the fe
cal Ig has leaked through the inflamed epithelial membrane into the gut lum
en. Finally, Ig-containing cells were observed in mesenteric lymph nodes an
d in the spleen, suggesting that the fecal Ig is produced both systemically
and locally in the gut wall. In conclusion, the present results demonstrat
e that the level of IgM increases as colitis progresses. Also, the five rem
aining major Ig isotypes are increased in the gut lumen of scid mice with c
olitis, but the individual Ig types vary randomly during the course of the
disease. Thus, it is unlikely that immunoglobulins are involved in the immu
nopathogenesis of this model of colitis. (C) 2000 Academic Press.