RT Journal Article
SR Electronic
T1 Cyclic-di-GMP is required for corneal infection by <em>Pseudomonas aeruginosa</em> and modulates host immunity
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 098749
DO 10.1101/098749
A1 Joey Kuok Hoong Yam
A1 Thet Tun Aung
A1 Song Lin Chua
A1 Yingying Cheng
A1 Gurjeet Singh Kohli
A1 Jianuan Zhou
A1 Florentin Constancias
A1 Yang Liu
A1 Zhao Cai
A1 May Margarette Santillan Salido
A1 Daniela I. Drautz-Moses
A1 Scott A. Rice
A1 Stephan Christoph Schuster
A1 Bin Wu
A1 Staffan Kjelleberg
A1 Tim Tolker-Nielsen
A1 Roger W. Beuerman
A1 Michael Givskov
A1 Liang Yang
YR 2017
UL http://biorxiv.org/content/early/2017/01/06/098749.abstract
AB Biofilms are extremely tolerant toward antimicrobial treatment and host immune clearance due to their distinct physiology and protection by extracellular polymeric substances. Bis-(3´-5´)-cyclic dimeric guanosine monophosphate (c-di-GMP) is an essential messenger that regulates biofilm formation by a wide range of bacteria. However, there is a lack of physiological characterization of biofilms in vivo as well as the roles of c-di-GMP signaling in mediating host-biofilm interactions. Here, we employed dual RNA-Seq to characterize the host and pathogen transcriptomes during Pseudomonas aeruginosa infection using a mouse keratitis model. In vivo P. aeruginosa biofilms maintained a distinct physiology compared with in vitro P. aeruginosa biofilms, with enhanced virulence and iron uptake capacity. C-di-GMP synthesis was enhanced in P. aeruginosa cells in vivo, potentially due to down-regulation of the expression of several phosphodiesterases (e.g., DipA, NbdA). Increased intracellular c-di-GMP levels were required for long-term ocular colonization of P. aeruginosa and impaired host innate immunity.