Open AccessY ersinia pseudotuberculosis uses A il and YadA to circumvent neutrophils by directing Y op translocation during lung infection
Author(s) -
Paczosa Michelle K.,
Fisher Michael L.,
MaldonadoArocho Francisco J.,
Mecsas Joan
Publication year - 2014
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12219
Subject(s) - spleen , yersinia pseudotuberculosis , virulence , bacterial adhesin , biology , lung , chromosomal translocation , microbiology and biotechnology , mutant , immunology , medicine , gene , biochemistry
Summary A Y ersinia pseudotuberculosis ( Yptb ) murine model of lung infection was previously developed using the serotype III IP 2666 NdeI strain, which robustly colonized lungs but only sporadically disseminated to the spleen and liver. We demonstrate here that a serotype Ib Yptb strain, IP 32953, colonizes the lungs at higher levels and disseminates more efficiently to the spleen and liver compared with IP 2666 NdeI . The role of adhesins was investigated during IP 32953 lung infection by constructing isogenic Δ ail , Δ inv , Δ psaE and Δ yadA mutants. An IP 32953Δ ail Δ yadA mutant initially colonized but failed to persist in the lungs and disseminate to the spleen and liver. Yptb expressing these adhesins selectively bound to and targeted neutrophils for translocation of Y ops. This selective targeting was critical for virulence because persistence of the Δ ail Δ yadA mutant was restored following intranasal infection of neutropenic mice. Furthermore, A il and YadA prevented killing by complement‐mediated mechanisms during dissemination to and/or growth in the spleen and liver, but not in the lungs. Combined, these results demonstratethat A il and YadA are critical, redundant virulence factors during lung infection, because they thwart neutrophils by directing Y op‐translocation specifically into these cells.