Adhesins and Host Serum Factors Drive Yop Translocation by Yersinia into Professional Phagocytes during Animal Infection

作者：Maldonado Arocho Francisco J; Green Carlos; Fisher Michael L; Paczosa Michelle K; Mecsas Joan^*

来源：PLoS Pathogens, 2013, 9(6): e1003415.

DOI：10.1371/journal.ppat.1003415

Yersinia delivers Yops into numerous types of cultured cells, but predominantly into professional phagocytes and B cells during animal infection. The basis for this cellular tropism during animal infection is not understood. This work demonstrates that efficient and specific Yop translocation into phagocytes by Yersinia pseudotuberculosis (Yptb) is a multifactorial process requiring several adhesins and host complement. When WT Yptb or a multiple adhesin mutant strain, Delta ail Delta inv Delta yadA, colonized tissues to comparable levels, Delta ail Delta inv Delta yadA translocated Yops into significantly fewer cells, demonstrating that these adhesins are critical for translocation into high numbers of cells. However, phagocytes were still selectively targeted for translocation, indicating that other bacterial and/or host factors contribute to this function. Complement depletion showed that complement-restricted infection by Delta ail Delta inv Delta yadA but not WT, indicating that adhesins disarm complement in mice either by prevention of opsonophagocytosis or by suppressing production of proinflammatory cytokines. Furthermore, in the absence of the three adhesins and complement, the spectrum of cells targeted for translocation was significantly altered, indicating that Yersinia adhesins and complement direct Yop translocation into neutrophils during animal infection. In summary, these findings demonstrate that in infected tissues, Yersinia uses adhesins both to disarm complement-dependent killing and to efficiently translocate Yops into phagocytes.

• 出版日期2013-6