Disease relevance of yopP

• It is shown in this report that Yersinia enterocolitica induces apoptosis in macrophages and that this effect depends on YopP [1].
• YopP shows a high level of sequence similarity with AvrRxv, an avirulence protein from Xanthomonas campestris, a plant pathogen that induces programmed cell death in plant cells [1].
• The effects of YopP on the immune response were studied by a Yersinia Ag-independent approach using bacteria that translocate the well-characterized model Ag listeriolysin O of Listeria monocytogenes via their type III secretion system [2].

High impact information on yopP

• Yersinia enterocolitica induces apoptosis in macrophages by a process requiring functional type III secretion and translocation mechanisms and involving YopP, presumably acting as an effector protein [1].
• In this study, we explored the mechanism by which YopP succeeds to simultaneously disrupt several of these key signaling pathways of innate immunity [3].
• It is shown for the first time that YopP not only counteracts the innate immune defense but also inhibits the adaptive immune system by suppressing the development of an effective CD8 T cell response in a mouse model [2].
• PU5-1.8 macrophages were infected either with an avirulent (pYV(-)), a wild type (pYV(+)), or two knockout (yopP(-) and yopM(-)) mutants of Y. enterocolitica [4].
• YopP participates to this inhibition, whereas another pYV-encoded factor appears to also be involved in this down-regulation [4].

Biological context of yopP

• This finding supports the idea that YopP/J induces apoptosis by directly acting on cell death pathways, rather than being the mere consequence of gene induction inhibition in combination with microbial stimulation of the macrophage [5].
• Disruption of the catalytic core of YopP abolished the rapid generation of tBid, thereby hampering induction of apoptosis by Y. enterocolitica [5].
• Transfection of J774A.1 macrophages with YopP induced a moderate, but significant degree of apoptosis (40-50% of transfected cells) [6].
• This effect was strongly enhanced by additional initiation of LPS signaling (80-90%), indicating a synergism between LPS-induced signal transduction and inhibition of NF-kappaB by YopP [6].
• In contrast, VopP, which is encoded by a pathogenicity island on chromosome 2 and is homologous to the Yersinia YopP, was secreted via the TTSS2 pathway [7].

Anatomical context of yopP

• In an initial period (</=4 h) Toll-like receptor 4 (TLR4) signaling is required for Yersinia enterocolitica YopP-induced dendritic cell (DC) death [8].
• In addition, we found that high-virulence strains inject more YopP into the cytosol of eukaryotic target cells than do low-virulence strains [9].
• While T-cell proliferation was partially affected by infection of DC with plasmid-cured and YopP-deficient Yersinia mutant strains, no T-cell proliferation occurred after infection of DC with wild-type Y. enterocolitica [10].
• Both Inv and YopP appear to modulate gene expression in order to subvert epithelial cell functions involved in innate immunity [11].

Associations of yopP with chemical compounds

• We extended the results of Ruckdeschel et al. and found that on the basis of the presence or absence of arginine-143 of YopP (K. Ruckdeschel, K. Richter, O. Mannel, and J. Heesemann, Infect. Immun. 69:7652-7662, 2001) all the Y. enterocolitica strains used fell into two groups, which correlate with the low- and high-virulence phenotypes [9].

References