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Stenotrophomonas maltophilia mutant lacking flagella remains virulent in DBA/2N mice but is less efficient in stimulating TNF-α expression
Author(s) -
Arianna Pompilio,
Valentina Crocetta,
Giovanni Di Bonaventura
Publication year - 2018
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1093/femsle/fny205
Subject(s) - virulence , stenotrophomonas maltophilia , microbiology and biotechnology , mutant , biology , stenotrophomonas , pathogenesis , flagellum , motility , lung , tumor necrosis factor alpha , wild type , persistence (discontinuity) , cytokine , bacteria , immunology , pseudomonas aeruginosa , gene , medicine , pseudomonas , biochemistry , genetics , geotechnical engineering , engineering
To understand the role of flagella of Stenotrophomonas maltophilia in lung infections, DBA/2N mice were challenged with aflagellate fliI- mutant and colonization, invasion and persistence, lung damage and inflammatory response compared, on days 1 and 3 post-exposure (p.e.), with that of the isogenic wild-type (wt). Following exposure to nebulized bacterial suspension, mice infected with wt and fliI- strains showed a comparable trend in body weight change, pulmonary persistence, lung damage and mortality rate over the study period considered. Interestingly, although on day 1 p.e. both strains colonized near all the spleens, on day 3 p.e. wt strain persisted in 40% of spleens, whereas fliI- mutant was completely cleared. No significant differences were found in MIP-2, IFN-γ and IL-6 pulmonary levels between groups over time, except for TNF-α whose levels on day 1 p.e. were significantly higher in mice infected with flagellated wt strain. Overall, our results indicate that in S. maltophilia flagella and motility might not represent virulence traits involved in the pathogenesis of lung infection. However, the evidence for a specific flagellar-induced TNF-α response warrants further study.

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