Yersinia pestis Ail: multiple roles of a single protein

Yersinia pestis is one of the most virulent bacteria identified. It is the causative agent of plague-a systemic disease that has claimed millions of human lives throughout history. Y. pestis survival in insect and mammalian host species requires fine-tuning to sense and respond to varying environmen...

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Published inFrontiers in cellular and infection microbiology Vol. 2; p. 103
Main Authors Kolodziejek, Anna M, Hovde, Carolyn J, Minnich, Scott A
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 2012
Subjects
Adhesion
Ail
Animals
Bacterial Adhesion
Bacterial Outer Membrane Proteins - metabolism
Complement System Proteins - immunology
Humans
Immune Evasion
invasion
Microbiology
Neutrophils - immunology
OmpX
Virulence
Virulence Factors - metabolism
Yersinia pestis
Yersinia pestis - pathogenicity
OmpX
invasion
virulence
Ail
T3SS
adhesion
Yersinia pestis
serum resistance
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Summary:Yersinia pestis is one of the most virulent bacteria identified. It is the causative agent of plague-a systemic disease that has claimed millions of human lives throughout history. Y. pestis survival in insect and mammalian host species requires fine-tuning to sense and respond to varying environmental cues. Multiple Y. pestis attributes participate in this process and contribute to its pathogenicity and highly efficient transmission between hosts. These include factors inherited from its enteric predecessors; Y. enterocolitica and Y. pseudotuberculosis, as well as phenotypes acquired or lost during Y. pestis speciation. Representatives of a large Enterobacteriaceae Ail/OmpX/PagC/Lom family of outer membrane proteins (OMPs) are found in the genomes of all pathogenic Yersiniae. This review describes the current knowledge regarding the role of Ail in Y. pestis pathogenesis and virulence. The pronounced role of Ail in the following areas are discussed (1) inhibition of the bactericidal properties of complement, (2) attachment and Yersinia outer proteins (Yop) delivery to host tissue, (3) prevention of PMNL recruitment to the lymph nodes, and (4) inhibition of the inflammatory response. Finally, Ail homologs in Y. enterocolitica and Y. pseudotuberculosis are compared to illustrate differences that may have contributed to the drastic bacterial lifestyle change that shifted Y. pestis from an enteric to a vector-born systemic pathogen.
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Reviewed by: Eric Krukonis, University of Michigan, USA; Mikael Skurnik, University of Helsinki, Finland
Edited by: Matthew Francis, Umeå University, Sweden
ISSN:2235-2988
2235-2988
DOI:10.3389/fcimb.2012.00103