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Literature summary for 3.4.23.48 extracted from

  • Banerjee, S.K.; Huckuntod, S.D.; Mills, S.D.; Kurten, R.C.; Pechous, R.D.
    Modeling pneumonic plague in human precision-cut lung slices highlights a role for the plasminogen activator protease in facilitating type 3 secretion (2019), Infect. Immun., 87, e00175-19 .
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Yersinia pestis P17811
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-

Synonyms

Synonyms Comment Organism
Pla
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Yersinia pestis
plasminogen activator protease Pla
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Yersinia pestis

General Information

General Information Comment Organism
malfunction deletion of Pla results in a decreased Yersinia pestis bacterial burden in the host lung and failure to progress into the lethal proinflammatory phase of disease. Deletion of Pla does not alter adherence to and/or secretion into THP-1 cells. Infection of human precision-cut lung slices (hPCLS) with the knockout DELTApla strain results in significantly reduced Yersinia outer protein (Yop) translocation early after infection and continuing to 4 hours-post-infection. And deletion of Pla results in decreased Yersinia pestis T3S into alveolar macrophages in vivo during pneumonic plague. Addition of Pla to Yersinia pestis lacking all five known adhesins partially restores adherence and Yop delivery to macrophages derived from the human monocytic cell line THP-1 and human epithelial type 2 (HEp-2) cells, suggesting that Pla may contribute to adherence and Yop translocation in vitro Yersinia pestis
physiological function the activity of the plasminogen activator protease Pla is the key to the progression of infection of Yersinia pestis in humans. Enzyme Pla facilitates type 3 secretion into primary alveolar macrophages but not into the commonly used THP-1 cell line. Analysis of the role of Pla in promoting optimal type 3 secretion using primary human tissue with relevant host cell heterogeneity in human precision-cut lung slices, a model of living tissue. Pla is a key player in the early host/pathogen interactions and a key virulence factor. Pla plays a role in adherence to alveolar macrophages that may not be detected using immortalized cell lines Yersinia pestis