Dataset Information

Peer pressure from a Proteus mirabilis self-recognition system controls participation in cooperative swarm motility

ABSTRACT: A resident of animal intestines, Proteus mirabilis is a major cause of catheter-associated urinary tract infections and can cause recurrent, persistent infections. Swarming, which is a collective behavior that promotes centimeter-scale population migration, is implicated in colonization of bladders and kidneys. A regulatory factor of swarming is kin recognition, which involves the transfer of a self-identity protein from one cell into a physically adjacent neighboring cell. However, how kin recognition regulates swarming was previously unclear. We have now shown a mechanism linking kin recognition, swarm migration, and antibiotics tolerance: cells induce a transient antibiotics-tolerant, persister-like state in adjacent non-identical cells which in turn prevents non-identical cells from continuing to participate in collective swarming. These affected non-identical cells continue to exhibit large-scale gene expression suggesting an active shift into a different expression state. These data provide two key insights for the field. First, kin recognition can be a regulatory mechanism that acts with spatial and temporal precision. Second, induction into an antibiotics-tolerant state, instead of occurring stochastically, can be physically and spatially regulated by neighboring cells. These insights highlight the importance of further developing four-dimensional (time and X-, Y-, Z-axes) model systems for interrogating cell-cell signaling and control in microbial populations.

ORGANISM(S): Proteus mirabilis

PROVIDER: GSE131647 | GEO | 2019/05/23

REPOSITORIES: GEO

ACCESS DATA

Similar Datasets

Project description:Kaiser2014 - Salmonella persistence after ciprofloxacin treatment The model describes the bacterial tolerance to antibiotics. Using a mouse model for Salmonella diarrhea, the authors have found that bacterial persistence occurs in the presence of the antibiotic ciprofloxacin because Salmonella can exist in two different states. One, the fast-growing population that spreads in the host's tissues and the other, slow-growing "persister" population that hide out inside dendritic cells of the host's immune system and cannot be attacked by the antibiotics. However, this can be killed by adding agents that directly stimulate the host's immune defense. This model is described in the article: Cecum lymph node dendritic cells harbor slow-growing bacteria phenotypically tolerant to antibiotic treatment. Kaiser P, Regoes RR, Dolowschiak T, Wotzka SY, Lengefeld J, Slack E, Grant AJ, Ackermann M, Hardt WD. PLoS Biol. 2014 Feb 18;12(2):e1001793. Abstract: In vivo, antibiotics are often much less efficient than ex vivo and relapses can occur. The reasons for poor in vivo activity are still not completely understood. We have studied the fluoroquinolone antibiotic ciprofloxacin in an animal model for complicated Salmonellosis. High-dose ciprofloxacin treatment efficiently reduced pathogen loads in feces and most organs. However, the cecum draining lymph node (cLN), the gut tissue, and the spleen retained surviving bacteria. In cLN, approximately 10%-20% of the bacteria remained viable. These phenotypically tolerant bacteria lodged mostly within CD103⁺CX₃CR1⁻CD11c⁺ dendritic cells, remained genetically susceptible to ciprofloxacin, were sufficient to reinitiate infection after the end of the therapy, and displayed an extremely slow growth rate, as shown by mathematical analysis of infections with mixed inocula and segregative plasmid experiments. The slow growth was sufficient to explain recalcitrance to antibiotics treatment. Therefore, slow-growing antibiotic-tolerant bacteria lodged within dendritic cells can explain poor in vivo antibiotic activity and relapse. Administration of LPS or CpG, known elicitors of innate immune defense, reduced the loads of tolerant bacteria. Thus, manipulating innate immunity may augment the in vivo activity of antibiotics. This model is hosted on BioModels Database and identified by: MODEL1312170001. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Dataset Information

Peer pressure from a Proteus mirabilis self-recognition system controls participation in cooperative swarm motility

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure