The Pla surface protease of Yersinia pestis activates human plasminogen and is a central virulence factor in bubonic and pneumonic plague. Pla is a transmembrane beta-barrel protein and member of the omptin family of outer membrane proteases which require bound lipopolysaccharide (LPS) to be proteolytically active. Plasminogen activation and autoprocessing of Pla were dramatically higher in Y. pestis cells grown at 37 degrees C than in cells grown at 20 degrees C; the difference in enzymatic activity by far exceeded the increase in the cellular content of the Pla protein. Y. pestis modifies its LPS structure in response to growth temperature. We purified His(6)-Pla under denaturing conditions and compared various LPS types for their capacity to enhance plasmin formation by His(6)-Pla solubilized in detergent. Reactivation of His(6)-Pla was higher with Y. pestis LPSs isolated from bacteria grown at 37 degrees C than with LPSs from cells grown at 25 degrees C. Lack of O antigens and the presence of the outer core region as well as a lowered level of acylation in LPS were found to enhance the Pla-LPS interaction. Genetic substitution of arginine 138, which is part of a three-dimensional protein motif for binding to lipid A phosphates, decreased both the enzymatic activity of His(6)-Pla and the amount of Pla in Y. pestis cells, suggesting the importance of the Pla-lipid A phosphate interaction. The temperature-induced changes in LPS are known to help Y. pestis to avoid innate immune responses, and our results strongly suggest that they also potentiate Pla-mediated proteolysis.
Infect Immun. 2010 Jun;78(6):2644-52.

Guinea-pigs were infected subcutaneously or by respiratory challenge with plasmid-containing (pPst+pCad+pFra+) Yersinia pestis strain 358 and its pPst-pCad+pFra+, pPst+pCad+pFra- and pPst- pCad+pFra- derivatives, grown in vitro at 28°C or at 37°C. Lack of plasmid pPst did not lead to an increase in LD50 with either route of challenge. When the virulence of the four Y. pestis strains grown at the two temperatures was compared, the LD50 values of those grown at 37°C were lower. Respiratory challenge with cultures grown at 37°C mimics the man-to-man pneumonic plague cycle. The average LD50 values decreased c. two-fold and 10-fold for pPst+ and pPst- Y. pestis variants, respectively. The data suggest that historical epidemic outbreaks of pneumonic plague in the human population residing in the Caucasus region where there are natural plague foci in common voles may have been caused by pPst- Y. pestis strains.
J. Med. Microbiol. 1996; 45 (6): 440-444.