Escherichia coli strain Nissle 1917 (
EcN) is as effective in maintaining remission in
ulcerative colitis as is treatment with
mesalazine. This study aims to evaluate murine models of acute and chronic intestinal
inflammation to study the antiinflammatory effect of
EcN in vivo. Acute
colitis was induced in mice with 2%
dextran-
sodium sulfate (DSS) in
drinking water.
EcN was administered from day -2 to day +7. Chronic
colitis was induced by transfer of CD4(+) CD62L(+) T lymphocytes from BALB/c mice in SCID mice.
EcN was administered three times/week from week 1 to week 8 after cell transfer. Mesenteric lymph node (MLN)
cytokine secretion (of
gamma interferon [IFN-gamma],
interleukin 5 [IL-5], IL-6, and IL-10) was measured by
enzyme-linked
immunosorbent assay. Histologic sections of the colon were analyzed by using a score system ranging from 0 to 4. Intestinal contents and homogenized MLN were cultured, and the number of E. coli-like colonies was determined.
EcN was identified by repetitive extragenic palindromic (REP) PCR.
EcN administration to DSS-treated mice reduced the secretion of proinflammatory
cytokines (IFN-gamma, 32,477 +/- 6,377 versus 9,734 +/- 1,717 [P = 0.004]; IL-6, 231 +/- 35 versus 121 +/- 17 [P = 0.02]) but had no effect on the mucosal
inflammation. In the chronic experimental
colitis of the transfer model,
EcN ameliorated the intestinal
inflammation (histology score, 2.7 +/- 0.2 versus 1.9 +/- 0.3 [P = 0.02]) and reduced the secretion of proinflammatory
cytokines. Translocation of
EcN and resident E. coli into MLN was observed in the chronic
colitis model but not in healthy controls. Administration of
EcN ameliorated acute and chronic experimental
colitis by modifying proinflammatory
cytokine secretion but had no influence on the acute DSS-induced
colitis. In this model, preexisting
colitis was necessary for translocation of
EcN and resident E. coli into MLN.