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Infection and Immunity, March 2002, p. 1453-1460, Vol. 70, No. 3
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.3.1453-1460.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Fraction 1 Antigen of Yersinia pestis in Inhibition of Phagocytosis

Yidong Du,1 Roland Rosqvist,2 and Åke Forsberg1,,2*

Division of NBC-Protection, Swedish Defence Research Agency, SE-901 82 Umeå ,1 Department of Molecular Biology, University of Umeå, S-901 87 Umeå, Sweden2

Received 12 July 2001/ Returned for modification 23 August 2001/ Accepted 5 December 2001

Yersinia pestis, the causative agent of plague, expresses a capsule-like antigen, fraction 1 (F1), at 37°C. F1 is encoded by the caf1 gene located on the large 100-kb pFra plasmid, which is unique to Y. pestis. F1 is a surface polymer composed of a protein subunit, Caf1, with a molecular mass of 15.5 kDa. The secretion and assembly of F1 require the caf1M and caf1A genes, which are homologous to the chaperone and usher protein families required for biogenesis of pili. F1 has been implicated to be involved in the ability of Y. pestis to prevent uptake by macrophages. In this study we addressed the role of F1 antigen in inhibition of phagocytosis by the macrophage-like cell line J774. The Y. pestis strain EV76 was found to be highly resistant to uptake by J774 cells. An in-frame deletion of the caf1M gene of the Y. pestis strain EV76 was constructed and found to be unable to express F1 polymer on the bacterial surface. This strain had a somewhat lowered ability to prevent uptake by J774 cells. Strain EV76C, which is cured for the virulence plasmid common to the pathogenic Yersinia species, was, as expected, much reduced in its ability to resist uptake. A strain lacking both the virulence plasmid and caf1M was even further hampered in the ability to prevent uptake and, in this case, essentially all bacteria (95%) were phagocytosed. Thus, F1 and the virulence plasmid-encoded type III system act in concert to make Y. pestis highly resistant to uptake by phagocytes. In contrast to the type III effector proteins YopE and YopH, F1 did not have any influence on the general phagocytic ability of J774 cells. Expression of F1 also reduced the number of bacteria that interacted with the macrophages. This suggests that F1 prevents uptake by interfering at the level of receptor interaction in the phagocytosis process.

* Corresponding author. Mailing address: Division of NBC-Protection, Swedish Defence Research Agency, SE-901 82 Umeå, Sweden. Phone: 46-90-106660. Fax: 46-90-106806. E-mail: ake.forsberg{at}foi.se.

Infection and Immunity, March 2002, p. 1453-1460, Vol. 70, No. 3
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.3.1453-1460.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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