Yersinia pseudotuberculosis uses Ail and YadA to circumvent neutrophils by directing Yop translocation during lung infection. (3rd November 2013)

• Record Type: Journal Article
• Authors: Paczosa, Michelle K.; Fisher, Michael L.; Maldonado‐Arocho, Francisco J.; Mecsas, Joan
• Is Part Of: Cellular microbiology. Volume 16:Number 2(2014:Feb.)
• Page Start: 247
• Page End: 268
• Publication Date: 2013-11-03
• Subjects: Microbiology -- Periodicals; Cytology -- Periodicals; Host-parasite relationships -- Periodicals; Microbiology -- Periodicals; Cells -- Periodicals; Microbiologie -- Périodiques; Microbiologie; Relation hôte-parasite; Cytologie; Cellule; Réponse cellulaire; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); 579.05
• DOI: 10.1111/cmi.12219
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>A <italic>Y</italic><italic>ersinia pseudotuberculosis (</italic><italic>Yptb</italic><italic>) </italic>murine model of lung infection was previously developed using the serotype III IP2666<sub>NdeI</sub> strain, which robustly colonized lungs but only sporadically disseminated to the spleen and liver. We demonstrate here that a serotype Ib <italic>Yptb</italic> strain, IP32953, colonizes the lungs at higher levels and disseminates more efficiently to the spleen and liver compared with IP2666<sub>NdeI</sub>. The role of adhesins was investigated during IP32953 lung infection by constructing isogenic Δ<italic>ail</italic><italic>, </italic>Δ<italic>inv</italic><italic>, </italic>Δ<italic>psaE</italic> and Δ<italic>yadA</italic> mutants. An IP32953Δ<italic>ail</italic>Δ<italic>yadA</italic> mutant initially colonized but failed to persist in the lungs and disseminate to the spleen and liver. <italic>Yptb</italic> expressing these adhesins selectively bound to and targeted neutrophils for translocation of Yops. This selective targeting was critical for virulence because persistence of the Δ<italic>ail</italic>Δ<italic>yadA</italic> mutant was restored following intranasal infection of neutropenic mice. Furthermore, Ail 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 Ail and YadA are critical, redundant virulence factors during lung infection, because they thwart neutrophils by directing Yop‐translocation specifically into these cells.</p> </abstract>