Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.04.02.716085

Particle Swarm Optimization with Random Forest Surrogates Modelling for Rational Design of Antimicrobial Fluoride Toothpaste Formulations against Clinically Significant Oral Pathogens

Abstract

To make effective antimicrobial toothpastes, you need to optimize many parts that work together. Creating new formulations the old-fashioned way takes a lot of time and money. This research formulates and substantiates a methodological framework that combines systematic antimicrobial susceptibility testing with Particle Swarm Optimization (PSO) to enhance toothpaste formulations against clinically significant oral pathogens. Using a D-optimal mixture design, we made 24 different toothpaste formulations by changing the type of fluoride (NaF, MFP, SnF2), the concentration of fluoride (1000-1500 ppm), the concentration of SLS (0.5-2.5%), the type of abrasive (silica, calcium carbonate, dicalcium phosphate), and the concentration of abrasive (10-30%). We used agar well diffusion and minimum inhibitory concentration (MIC) tests to see how well the drugs worked against Streptococcus mutans ATCC 25175, Porphyromonas gingivalis ATCC 33277, and Lactobacillus acidophilus ATCC 4356. A Random Forest surrogate model was trained on 120 experimental data points (24 formulations x 5 concentrations) and validated through 10-fold cross-validation. Multi-objective PSO was used to improve the effectiveness of antimicrobials, the availability of fluoride, and the cost of the formulation. Chosen PSO-predicted formulations underwent experimental validation. The antimicrobial activity changed a lot (p < 0.001) depending on the formulation parameters. The optimized formulation (sodium fluoride 1120 ppm, SLS 2.3%, hydrated silica 18%, pH 7.2) showed 28.4 {+/-} 1.2 mm of inhibition against S. mutans, 26.8 {+/-} 1.4 mm against P. gingivalis, and 24.2 {+/-} 1.1 mm against L. acidophilus. These were improvements of 18.5%, 22.3%, and 19.8%, respectively, over the best commercial comparator. Experimental validation corroborated PSO predictions with a mean absolute error of 5.2%. Multi-objective Optimization found Pareto-optimal formulations that let you choose based on trade-offs between effectiveness, safety, and cost. Combining systematic experimental design with PSO gives a tested framework for making rational toothpaste formulations. This method significantly lowers the amount of work needed for experiments while also allowing for the Optimization of multiple competing formulation goals.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

ASUAI, C., Whilliki, O., Mayor, A., Victory, D., Imarah, O., Asuai, A., Irene, D., Merit, I., Hosni, H., Khan, M. I., Edwin, A. C., Destiny, I. E.. 2026-04-03. Particle Swarm Optimization with Random Forest Surrogates Modelling for Rational Design of Antimicrobial Fluoride Toothpaste Formulations against Clinically Significant Oral Pathogens. https://doi.org/10.64898/2026.04.02.716085

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Prevalent Integration of both Xenotropic and Ecotropic Murine Leukemia Virus in the Human Genome of Xenografts

Humanized mouse models are widely used in medical research to represent human conditions (1, 2), but their fidelity could be compromised by mouse-originated infections. However, their susceptibility to mouse pathogens are rarely questioned (3). Here we screened 1,619 publicly available genomic sequencing runs from patient-derived xenograft (PDX) models for the integration of murine leukemia virus (MLV), a rodent retrovirus exists in the mouse genome as an endogenous retrovirus (4), within the human genome. We discovered substantial enrichment of human-MLV chimeric DNA in approximately 25% of them. Analyzing the human-MLV junctions, we found about 90% of them bearing the unmistakable hallmarks of retroviral integration, including the canonical MLV boundaries and the distinctive 4-bp target site duplications (5, 6). It was also assumed that mouse strains without the highly infectious Bxv1 provirus are safe from MLV contamination in xenografts (7, 8). However, we found many PDX models derived from Bxv1- strains, including the widely used NSG strain, are also contaminated by the supposedly rodent-specific ecotropic MLV (E-MLV). We further confirmed a complete E-MLV integrated into the human genome by both HiFi and sanger sequencing. Our discovery raises concerns that mouse-to-human retroviral transmission and integration is more common and less restrictive than previously appreciated. They support examination of MLV integration as a feature of humanized mouse models with implications on the fidelity of these models in recapitulating human cells and tissues. Our discovery also has underscored the importance of comprehensively inactivation of porcine endogenous retroviruses for the clinical application of xenotransplatation (9, 10).

microbiology↗

Necroptosis is a targetable driver of severe coronavirus pathogenesis

Human-pathogenic coronaviruses differ dramatically in pathogenicity but the underlying mechanisms are incompletely understood. Here, we demonstrate that highly pathogenic coronaviruses trigger necroptosis in the infected cells and lung tissues, whereas necroptosis is not detected in cells infected by seasonal coronavirus. Mechanistically, highly pathogenic coronaviruses produce Z-RNA, activate ZBP1 and initiates necroptotic cell death signaling, triggering necroinflammation and lung injury. In contrast, seasonal coronaviruses produce little to no Z-RNA, and do not activate necroptosis. Importantly, small-molecule inhibition of necroptosis attenuates inflammatory cytokine expression and markedly ameliorates lung damage in mice infected with all three highly pathogenic coronaviruses, independent of virus clearance. Overall, our study identifies necroptosis as a dominant mediator of coronavirus pathogenesis, and positions necroptosis blockade as a new therapeutic target against severe coronavirus diseases.

microbiology↗

POM121 regulates lentiviral nuclear import in a capsid-host factor-dependent manner

Lentiviruses such as human immunodeficiency virus 1 (HIV-1) access the nuclear lumen through the nuclear pore complex (NPC), a process coordinated by the interactions between the viral capsid and nucleoporins (NUPs). Here, using unbiased proteomic screens, we identified several capsid-associated NUPs, including POM121. Depletion of POM121 impaired HIV-1 infection in multiple cell lines and in primary CD4+ T cells, whereas equine infectious anaemia virus (EIAV) infection was enhanced, indicating that POM121 effect is virus-specific. A cytoplasmic carboxy-terminal fragment of POM121, containing its FG-rich region inhibited HIV-1 and a broader range of lentiviruses. Analysis of HIV-1 capsid mutants showed that physical interaction with POM121 does not predict functional dependence, as capsids retaining POM121 binding remained insensitive to its depletion. Strikingly, loss of cyclophilin A (CypA) completely abolished HIV-1 dependence on POM121, whereas depletion of CPSF6 produced only partial rescue, demonstrating that POM121 sensitivity is dictated by the broader network of capsid-host interactions. Finally, POM121 depletion impaired HIV-1 nuclear accumulation and selectively disrupted the nuclear import of other viral and cellular cargo. Together, these findings identify POM121 as a selective regulator of lentiviral nuclear entry whose functional contribution is determined by capsid and host-factor context.

microbiology↗