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Genetically Engineered Lactococcus lactis Secreting Murine IL‐10 Modulates the Functions of Bone Marrow‐Derived Dendritic Cells in the Presence of LPS
Author(s) -
Loos M.,
Remaut E.,
Rottiers P.,
De Creus A.
Publication year - 2009
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2008.02206.x
Subject(s) - lactococcus lactis , inflammation , immune system , secretion , bone marrow , chemistry , colitis , dendritic cell , microbiology and biotechnology , immunology , biology , bacteria , biochemistry , lactic acid , genetics
Oral delivery of IL‐10 by genetically modified Lactococcus lactis ( LL‐pTmIL10 ) has been shown to efficiently reduce intestinal inflammation in mice with chronic colitis, but the mechanisms involved have not been elucidated. It has been suggested that IL‐10 controls intestinal inflammation by inhibiting microbe‐induced activation of dendritic cells. We therefore investigated whether LL‐pTmIL10 can modulate the functions of bone marrow‐derived dendritic cells (BM‐DC) responding to LPS. Incubation of these cells with LL‐pTmIL10 or with the control strain LL‐pTREX reduced their ability to activate allogeneic T‐cell proliferation. However, in contrast to LL‐pTREX , LL‐pTmIL10 inhibited the LPS‐stimulated secretion of MCP‐1 by BM‐DC and reduced the synergistic up‐regulation of IL‐12/IL‐23p40. In addition, LL‐pTmIL10 treatment of LPS‐stimulated BM‐DC significantly inhibited their capacity to induce strong secretion of IL‐17 by CD4 + T cells. Our data suggest that the beneficial effects of LL‐pTmIL10 treatment during chronic colitis might involve inhibition of CD4 + Th17 cells and a reduced accumulation of these cells as well as other immune cells at the site of inflammation.