Reinhard Laubenbacher
Profile Url: reinhard-laubenbacher
Researcher at University of Florida College of Medicine
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Video Abstract (AI generated)
Paper
Preprint
As common commensals residing on mucosal tissues, Lactobacillus species are known to encourage health, while recent findings highlight the pathogenic roles of Streptococcus species in these environments. In this study we used a combination of in vivo imaging experiments and computational modeling to explore biofilm interactions between Streptococcus oralis, an accessory pathogen in oral Candidiasis, and Lactobacillus paracasei, an organism with known probiotic properties. A computational agent-based model was created where the two species only interact by competing for space and nutrients. Quantification of bacterial growth in live biofilms indicated that S. oralis biomass and cell numbers were much lower than predicted by the model. Two subsequent models were then created to examine more complex interactions between these species, one where L. paracasei secretes a surfactant, and another where L. paracasei secretes an inhibitor of S. oralis growth. Further biofilm experiments support the hypothesis that L. paracasei may secrete an inhibitor of S. oralis growth, although they do not exclude that a surfactant could also be involved. This contribution shows how agent-based modeling and experiments can be used in synergy to address multiple species biofilm interactions, with important roles in mucosal health and disease.
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Molecular Microbiology, 2018-09-16
Video Abstract (AI generated)
Paper
Preprint
Molecular Microbiology
Biological systems require precise copper homeostasis enabling metallation of cuproproteins while preventing metal toxicity. In bacteria, sensing, transport and storage molecules act in coordination to fulfill these roles. However, there is not yet a kinetic schema explaining the system integration. Here, we report a model emerging from experimental and computational approaches that describes the dynamics of copper distribution in Pseudomonas aeruginosa. Based on copper uptake experiments, a minimal kinetic model describes well the copper distribution in the wild type bacteria but is unable to explain the behavior of the mutant strain lacking CopA1, a key Cu+ efflux ATPase. The model was expanded through an iterative hypothesis-driven approach, arriving to a mechanism that considers the induction of compartmental pools and the parallel function of CopA and Cus efflux systems. Model simulations support the presence of a periplasmic copper storage with a crucial role under dyshomeostasis conditions in P. aeruginosa. Importantly, the model predicts not only the interplay of periplasmic and cytoplasmic pools but also the existence of a threshold in the concentration of external copper beyond which cells lose their ability to control copper levels.