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(Journal of Leukocyte Biology. 2002;71:238-246.)
© 2002 by Society for Leukocyte Biology

Bacterial metabolite interference with maturation of human monocyte-derived dendritic cells

Marcus D. Säemann*, Ornella Parolini*, Georg A. Böhmig{dagger}, Peter Kelemen*, Peter-Michael Krieger*, Josef Neumüller{ddagger}, Katharina Knarr*, Willibald Kammlander*, Walter H. Hörl{dagger}, Christos Diakos*, Karl Stuhlmeier§ and Gerhard J. Zlabinger*

* Institute of Immunology,
{dagger} Department of Internal Medicine III, and
{ddagger} Institute of Histology, University of Vienna, Austria; and
§ Ludwig Boltzmann Institute for Rheumatology, Vienna, Austria

Correspondence: Gerhard Zlabinger, Institute of Immunology, University of Vienna, Borschkegasse 8a, A-1090 Vienna, Austria. E-mail: Gerhard.Zlabinger{at}univie.ac.at

Dendritic cells (DC), the most potent APC, are central to antimicrobial immunity. Because of evolutionary pressure, it is reasonable that pathogens have evolved strategies to also subvert this host-defense mechanism. In the present study, we describe a novel way of bacterial interference with DC maturation. The bacterial metabolite n-butyrate, which occurs physiologically in high concentrations in the gastrointestinal tract and has well-known anti-inflammatory effects, is able to prevent LPS-induced maturation of DC resulting in a reduced capability to stimulate T cells. In particular, n-butyrate prevents homotypic DC clustering, inhibits IL-12 while sparing IL-10 production, and at the molecular level, blocks NF-{kappa}B translocation. These results demonstrate efficient targeting of DC function by a bacterial metabolite, which might explain the particular type of immune responsiveness in the presence of this bacterial agent as exemplified in the gastrointestinal tract.

Key Words: bacteria • host defense • cytokine • cellular differentiation • immunomodulator




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