Parameter Estimation of Dynamical System Based on Bacterial Foraging Algorithm

We consider parameter estimation in dynamical systems from finite-time, partially observed trajectories. Rather than calibrating parameters within a prescribed model structure, we formulate parameter estimation as an inverse problem for a parameter-to-observation operator and learn its inverse directly from data using deep neural networks. Under appropriate identifiability assumptions, this inverse map is well-defined and continuous, making it amenable to approximation by neural networks. We discuss identifiability, stability, and noise sensitivity of the inverse problem and provide a simple error decomposition that separates approximation error from noise amplification. Numerical experiments on linear, nonlinear, nonautonomous, partially observed, noisy, and chaotic systems demonstrate accurate parameter recovery. For chaotic systems, recovery is validated through agreement of invariant dynamical quantities rather than pointwise trajectories.

Quorum sensing (QS) is a process of cell-to-cell communication that bacteria use to orchestrate collective behaviors. QS relies on the cell-density-dependent production, accumulation, and receptor-mediated detection of extracellular signaling molecules called autoinducers (AIs). Gram-negative bacteria commonly use N-acyl homoserine lactones (AHLs) as their AIs, and they are detected by LuxR-type receptors. Often, LuxR-type receptors are insoluble when not bound to a cognate AI. In this report, we show that LuxR-type receptors are encoded on phage genomes, and in the cases we tested, the phage LuxR-type receptors bind to and are solubilized specifically by the AHL AI produced by the host bacterium. We do not yet know the viral activities that are controlled by these phage QS receptors; however, our observations, coupled with recent reports, suggest that their occurrence is more widespread than previously appreciated. Using receptor-mediated detection of QS AIs could enable phages to garner information concerning the population density status of their bacterial hosts. We speculate that such information can be exploited by phages to optimize the timing of execution of particular steps in viral infection.IMPORTANCE Bacteria communicate with chemical signal molecules to regulate group behaviors in a process called quorum sensing (QS). In this report, we find that genes encoding receptors for Gram-negative bacterial QS communication molecules are present on genomes of viruses that infect these bacteria. These viruses are called phages. We show that two phage-encoded receptors, like their bacterial counterparts, bind to the communication molecule produced by the host bacterium, suggesting that phages can "listen in" on their bacterial hosts. Interfering with bacterial QS and using phages to kill pathogenic bacteria represent attractive possibilities for development of new antimicrobials to combat pathogens that are resistant to traditional antibiotics. Our findings of interactions between phages and QS bacteria need consideration as new antimicrobial therapies are developed.

Quorum sensing (QS) is a cell-to-cell communication mechanism that occurs between inter- and intra-bacterial species and is regulated by signaling molecules called autoinducers (AIs). It has been suggested that probiotics can exert a QS inhibitory effect through their metabolites. To provide an overview of (1) the anti-QS activity of probiotics and its mechanism against foodborne pathogenic and spoilage bacteria; (2) the potential role of the QS of probiotics in gut health; and (3) the impact of microencapsulation on QS. Lactobacillus species have been extensively studied for their anti-QS activity and have been found to effectively disrupt QS in vitro. However, their effectiveness in a food matrix is yet to be determined as they interfere with the AI receptor or its synthesis. QS plays an important role in both the biofilm formation of probiotics and pathogenic bacteria. Moreover, in vitro and animal studies have shown that QS molecules can modulate cytokine responses and gut dysbiosis and maintain intestinal barrier function. In this scenario, microencapsulation was found to enhance AI activity. However, its impact on the anti-QS activity of probiotics and its underlying mechanism remains unclear. Probiotics are potential candidates to block QS activity in foodborne pathogenic and food spoilage bacteria. Microencapsulation increases QS efficacy. However, more research is still needed for the identification of the QS inhibitory metabolites from probiotics and for the elucidation of the anti-QS mechanism of probiotics (microcapsules and free cells) in food and the human gut.

Quorum sensing is a process of chemical communication that adjusts the genetic expression of certain important biological functions in a cell-density—dependent manner. Quorum sensing (QS) regulates important bacterial behaviors, such as production of virulence factors, formation of biofilm, and antibiotic resistance, via signaling molecules called autoinducers (AIs). Gram-negative bacteria typically use N-acyl homoserine lactones (AHLs) and S-adenosyl methionine (SAM) molecules as signaling molecules for communication with neighboring cells, while Gram-positive bacteria use oligopeptides for the same purpose. Autoinducer-2 (AI-2) is used as a signaling molecule by both Gram-negative and Gram-positive bacteria. These QS molecules are often involved in the expression of pathogenicity in different bacterial species. Because of the rapid emergence and dissemination of drug-resistant pathogens worldwide, antivirulence chemotherapies may be potential alternatives to the use of antibiotics, which kill bacteria but allow the emergence of resistance. Recently, successful strategies, employed for inhibition/manipulation of QS signaling, has brought real excitement for identifying novel advances to combat these life-threatening pathogens. This review highlights the QS systems used by Gram-negative and Gram-positive bacterial species and discusses promising QS inhibitor (QSI) molecules that may aid in designing novel antimicrobial therapeutics. Utilization of different QS components in the design and development of novel biotechnological products, such as biosensors, engineered microbial consortia, and anticancer molecules, is also addressed.

Bacterial cells communicate with one another using chemical signaling molecules. This phenomenon is termed quorum sensing (QS). QS in Klebsiella pneumoniae is mediated by the synthesis of interspecies autoinducer 2 (AI-2), a furanosyl borate diester molecule. The response of Type 2 QS to environmental cues such as carbon sources, the initial pH of the medium, and boracic acid was investigated in the present study using a Vibrio harveyi BB170 reporter assay and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis. The results show that glucose can affect AI-2 synthesis to the greatest extent, and 3.0% glucose can stimulate K. pneumoniae to produce more AI-2, with a four times increase in activity compared with that of the control culture. According to our previous research, Type 2 QS in K. pneumoniae is luxS dependent. Therefore, the close relationship between glucose concentration and luxS transcription level was confirmed with qRT-PCR technology. The results show that the response of QS to a fluctuating glucose concentration was observed as a change in the amount of luxS RNA transcripts. A maximum of luxS transcription appeared during the exponential growth phase when the glucose concentration was 30.0 g/L. At the same time, AI-2 production was also slightly impacted by the low initial pH. It is noteworthy that the addition of boracic acid at microdosage (0.1 g/L) can also induce AI-2 synthesis. Presumably, in K. pneumoniae, the 4,5-dihydroxy-2,3-pentanedione cyclizes by the addition of borate and loss of water, is hydrated, and is converted to the final AI-2 signaling molecule.

One of the key mechanisms enabling bacterial cells to create biofilms and regulate crucial life functions in a global and highly synchronized way is a bacterial communication system called quorum sensing (QS). QS is a bacterial cell-to-cell communication process that depends on the bacterial population density and is mediated by small signalling molecules called autoinducers (AIs). In bacteria, QS controls the biofilm formation through the global regulation of gene expression involved in the extracellular polymeric matrix (EPS) synthesis, virulence factor production, stress tolerance and metabolic adaptation. Forming biofilm is one of the crucial mechanisms of bacterial antimicrobial resistance (AMR). A common feature of human pathogens is the ability to form biofilm, which poses a serious medical issue due to their high susceptibility to traditional antibiotics. Because QS is associated with virulence and biofilm formation, there is a belief that inhibition of QS activity called quorum quenching (QQ) may provide alternative therapeutic methods for treating microbial infections. This review summarises recent progress in biofilm research, focusing on the mechanisms by which biofilms, especially those formed by pathogenic bacteria, become resistant to antibiotic treatment. Subsequently, a potential alternative approach to QS inhibition highlighting innovative non-antibiotic strategies to control AMR and biofilm formation of pathogenic bacteria has been discussed.

Bacteria are able to produce and act in response to minute diffusible molecules called autoinducers (AI). These molecules amass as cell density enhancements and regulate the expression of set of genes to control diverse physiological functions by quorum sensing (QS). Several species of bacteria swap signal molecules to assist checking their own population densities. Until recently, it was contemplated that QS was an unusual phenomenon restricted to not many microbial species. Nevertheless, numerous novel exemplars of interbacterial and intrabacterial signaling mechanisms are documented. Amongst them, acyl-homoserine lactone (AHL) and QS signaling systems are perhaps the best implicated diverse chemical languages used by both Gram-positive and Gram negative bacteria respectively. QS systems have primarily smudged the difference involving unicellular and multicellular life forms. Several QS systems exceptionally essential to medicine and agriculture. These QS microbes could be undoubtedly expensive tools for biologists to inquire and comprehend the progress of cooperation and cell to cell communication, wherein the realistic applications of this acquaintance will befall well-known in conjunction with basic acquaintance.

Inhibition of quorum sensing, biofilm formation, and virulence-related characteristics in shrimp pathogenic Vibrio campbellii by rambutan (Nephelium lappaceum L. cv. Rong Rian) peel extract.

Developments in strategies for Quorum Sensing virulence factor inhibition to combat bacterial drug resistance

Synthesis of antimicrobial glucosamides as bacterial quorum sensing mechanism inhibitors

Bacterial populations use a cell-to-cellcommunication system tocoordinate community-wide regulation processes, which is termed quorumsensing (QS). Autoinducer-2 (AI-2) is a universal signal molecule that mediates inter-and intraspecies QS systems among different bacteria. In this study,the effects of exogenous addition of AI-2 synthesized in vitro onphysiological behaviors and proteome were investigated in lactic acidbacteria strains. Exogenous AI-2 had a concentration-dependent effecton the Enterococcus faecium 8-3 celldensity. There was no significant influence on biofilm formation andindividual morphology of cells upon 60 μM AI-2 addition in E. faecium 8-3 and Lactobacillus fermentum 2-1.However, it improved the acid and alkali resistance of E. faecium 8-3. With the addition of AI-2, 15 differentiallyexpressed proteins were identified in E. faecium 8-3, which participate in RNA transport signaling, RNA polymerase,ribosome, oxidative phosphorylation, cysteine and methionine metabolism,pyrimidine metabolism, ATP-binding cassette (ABC) transporters, purinemetabolism, biosynthesis of the amino acid pathway, etc. Among them,the expression of 5-methylthioadenosine/S-adenosylhomocysteinenucleosidase, which is known to be involved in AI-2 synthesis andcysteine and amino acid metabolism, was upregulated. These findingswill lay the foundation to clarify the mechanism of cell-to-cell communicationand bacterial physiological behaviors mediated by AI-2.

Structure‐Based Discovery and Experimental Verification of Novel AI‐2 Quorum Sensing Inhibitors against <i>Vibrio harveyi</i>

Initial detection of the quorum sensing autoinducer activity in the rumen of goats in vivo and in vitro

Unveiling quorum sensing mechanisms: Computational docking and dynamics of bacterial receptors and ligands

A biofilm is an assemblage of microbial cells attached to a surface and encapsulated in an extracellular polymeric substance (EPS) matrix. The formation of a biofilm is one of the important mechanisms of bacterial resistance, which not only leads to hard-to-control bacterial infections in humans and animals but also enables bacteria to be a major problem in various fields, such as food processing, wastewater treatment and metalworking. Quorum sensing (QS) is a bacterial cell-to-cell communication process that depends on the bacterial population density and is mediated by small diffusible signaling molecules called autoinducers (AIs). Bacteria use QS to regulate diverse arrays of functions, including virulence and biofilm formation. Therefore, the interference with QS by using QS inhibiting agents, including QS inhibitors (QSIs) and quorum quenching (QQ) enzymes, to reduce or even completely repress the biofilm formation of pathogenic bacteria appears to be a promising approach to control bacterial infections. In this review, we summarize the mechanisms of QS-regulating biofilm formation and QS-inhibiting agents that control bacterial biofilm formation, strategies for the discovery of new QS inhibiting agents, and the current applications of QS-inhibiting agents in several fields to provide insight into the development of effective drugs to control pathogenic bacteria.