%0 Journal Article %T Serum resistance and phase variation of a nasopharyngeal non-typeable Haemophilus influenzae isolate %+ Karl-Franzens-Universität Graz %+ Institute of Molecular Biosciences %+ Ecologie et Evolution de la Résistance aux Antibiotiques / Ecology and Evolution of Antibiotics Resistance (EERA) %+ BioTechMed Graz [Graz, Autriche] %A Lichtenegger, Sabine %A Bina, Isabelle %A Durakovic, Sanel %A Glaser, Philippe %A Tutz, Sarah %A Schild, Stefan %A Reidl, Joachim %Z Work was supported by the Austrian Science Fund (FWF) ERA-NET FWF I 662-B09 to SL, and JR. Clinical NTHi isolates were donatedby AGES-Graz (Agentur Gesundheit und ErnaehrungssicherheitGmbH/Zentrum fuer lebensmittelbedingte Infektionskrankheiten,Dr. Georg Steindl, AGES Graz) and the Institute for Hygieneand Microbiology (Dr. Thien-Tri Lam, University of Wuerzburg,Germany) %< avec comité de lecture %@ 1438-4221 %J International Journal of Medical Microbiology %I Elsevier %V 307 %N 2 %P 139-146 %8 2017-02 %D 2017 %R 10.1016/j.ijmm.2017.01.005 %M 28179078 %K Haemophilus influenzae %K Phase variation %K Serum resistance %K lpsA %Z Life Sciences [q-bio]Journal articles %X Haemophilus influenzae harbours a complex array of factors to resist human complement attack. As non-typeable H. influenzae (NTHi) strains do not possess a capsule, their serum resistance mainly depends on other mechanisms including LOS decoration. In this report, we describe the identification of a highly serum resistant, nasopharyngeal isolate (NTHi23) by screening a collection of 77 clinical isolates. For NTHi23, we defined the MLST sequence type 1133, which matches the profile of a previously published invasive NTHi isolate. A detailed genetic analysis revealed that NTHi23 shares several complement evading mechanisms with invasive disease isolates. These mechanisms include the functional expression of a retrograde phospholipid trafficking system and the presumable decoration of the LOS structure with sialic acid. By screening the NTHi23 population for spontaneous decreased serum resistance, we identified a clone, which was about 103-fold more sensitive to complement-mediated killing. Genome-wide analysis of this isolate revealed a phase variation in the N'-terminal region of lpsA, leading to a truncated version of the glycosyltransferase (LpsA). We further showed that a NTHi23 lpsA mutant exhibits a decreased invasion rate into human alveolar basal epithelial cells. Since only a small proportion of the NTHi23 population expressed the serum sensitive phenotype, resulting from lpsA phase-off, we conclude that the nasopharyngeal environment selected for a population expressing the intact and functional glycosyltransferase. %G English %2 https://pasteur.hal.science/pasteur-03107776/document %2 https://pasteur.hal.science/pasteur-03107776/file/Lichteneggeret_al_Int_J_Med_Micr_2017.pdf %L pasteur-03107776 %U https://pasteur.hal.science/pasteur-03107776 %~ PASTEUR %~ CNRS %~ APHP %~ TEST-HALCNRS %~ UMR3525