PT  - JOURNAL ARTICLE
AU  - Landi, Alessia
AU  - Mari, Muriel
AU  - Kleiser, Svenja
AU  - Wolf, Tobias
AU  - Gretzmeier, Christine
AU  - Wilhelm, Isabel
AU  - Kiritsi, Dimitra
AU  - Thünauer, Roland
AU  - Geiger, Roger
AU  - Nyström, Alexander
AU  - Reggiori, Fulvio
AU  - Claudinon, Julie
AU  - Römer, Winfried
TI  - <em>Pseudomonas aeruginosa</em> lectin LecB impairs keratinocyte fitness by abrogating growth factor signalling
AID  - 10.26508/lsa.201900422
DP  - 2019 Dec 01
TA  - Life Science Alliance
PG  - e201900422
VI  - 2
IP  - 6
4099  - http://www.life-science-alliance.org/content/2/6/e201900422.short
4100  - http://www.life-science-alliance.org/content/2/6/e201900422.full
SO  - Life Sci. Alliance2019 Dec 01; 2
AB  - Lectins are glycan-binding proteins with no catalytic activity and ubiquitously expressed in nature. Numerous bacteria use 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, which extend beyond its role as an adhesion molecule. We found that LecB associates with insulin-like growth factor-1 receptor and dampens its signalling, leading to the arrest of cell cycle. In addition, we describe a novel LecB-triggered mechanism to down-regulate host cell receptors by showing that LecB leads to insulin-like growth factor-1 receptor internalisation and subsequent missorting towards intracellular endosomal compartments, without receptor activation. 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.