TY - JOUR T1 - <em>Pseudomonas aeruginosa</em> lectin LecB impairs keratinocyte fitness by abrogating growth factor signalling JF - bioRxiv DO - 10.1101/629972 SP - 629972 AU - Alessia Landi AU - Muriel Mari AU - Tobias Wolf AU - Svenja Kleiser AU - Christine Gretzmeier AU - Isabel Wilhelm AU - Dimitra Kiritsi AU - Roland Thünauer AU - Roger Geiger AU - Alexander Nyström AU - Fulvio Reggiori AU - Julie Claudinon AU - Winfried Römer Y1 - 2019/01/01 UR - http://biorxiv.org/content/early/2019/05/07/629972.abstract N2 - Lectins are glycan-binding proteins with no catalytic activity and ubiquitously expressed in nature. Numerous bacteria employ lectins to efficiently bind to epithelia, thus facilitating tissue colonisation. Wounded skin is one of the preferred niches for Pseudomonas aeruginosa, which has developed diverse strategies to impair tissue repair processes and promote infection.Here, we analyse the effect of the P. aeruginosa fucose-binding lectin LecB on human keratinocytes and demonstrate that it triggers events in the host, upon binding to fucosylated residues on cell membrane receptors, that extend beyond its role as an adhesion molecule. We found that LecB associates with several growth factor receptors and dampens their signalling pathways, leading to the arrest of cell cycle. Additionally, we describe a novel LecB-triggered mechanism to downregulate host cell receptors by showing that LecB leads to insulin-like growth factor receptor 1 internalisation, without receptor activation, and subsequent missorting towards intracellular endosomal compartments.Overall, these data highlight that LecB is a multitask virulence factor that, through subversion of several host pathways, has a profound impact on keratinocyte proliferation and survival. ER -