@article{mbs:/content/journal/jmm/10.1099/jmm.0.47437-0, author = "Adkins, Irena and Schulz, Sebastian and Borgmann, Stefan and Autenrieth, Ingo B. and Gröbner, Sabine", title = "Differential roles of Yersinia outer protein P-mediated inhibition of nuclear factor-kappa B in the induction of cell death in dendritic cells and macrophages", journal= "Journal of Medical Microbiology", year = "2008", volume = "57", number = "2", pages = "139-144", doi = "https://doi.org/10.1099/jmm.0.47437-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.47437-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", keywords = "DC, dendritic cells", keywords = "MKK, MAPK kinase", keywords = "NF-κB, nuclear factor-kappa B", keywords = "PI, propidium iodide", keywords = "MAPK, mitogen-activated protein kinase", keywords = "JNK, c-Jun N-terminal kinase", keywords = "CLSM, confocal laser scanning microscopy", abstract = " Yersinia outer protein P (YopP) induces cell death in macrophages and dendritic cells (DC). In DC this YopP-dependent cell death coincides with the inhibition of nuclear factor-kappa B (NF-κB) activation. However, as shown by measurement of propidium iodide uptake via disrupted cellular membranes, the preincubation of DC with several NF-κB inhibitors prior to infection with Yersinia did not restore the death-inducing capacity of a YopP-deficient Yersinia mutant. These results suggest that in contrast to macrophages, in DC the YopP-dependent inhibition of NF-κB activation is not causative for the induction of cell death. Instead, in DC, the inhibition of mitogen-activated protein kinases (MAPKs), in particular, p38 and c-Jun N-terminal kinase, prior to infection with a YopP-deficient Yersinia mutant substituted the death-inducing capacity of the Yersinia wild-type strain, indicating that the YopP-dependent inhibition of MAPKs mediates Yersinia-induced DC death. The differences between DC and macrophages in the mechanisms of cell death induction by YopP presented herein might be crucial for the function of these antigen-presenting cells.", }