ArticleBioengineering (Basel, Switzerland)2019
Influence of Pathogens and Mechanical Stimuli in Inflammation.
Article in Bioengineering (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Zirconium-based metal-organic frameworks for pathogen detection.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2026Review
- Fabrication of Chrysin-Loaded Hyaluronic Acid Decorated Niosomal Nanoparticles: Potential Anti-inflammatory and Anti-osteoclastic Effects on PBMCs of Rheumatoid Arthritis Patients.Advanced pharmaceutical bulletin · 2025Article
- Anti-Inflammatory and Antimicrobial Effects of Herbal Formulation Called Apo-Taat Using Extended-Spectrum ß-Lactamase-ProducingTheScientificWorldJournal · 2025Article
- Agent-based modeling of macrophage-fibroblast interactions in the immune response to biomaterials.PloS one · 2025Article
- CITED1 expression in odontogenic cysts.BMC oral health · 2024Article
- In Vitro Anti-Inflammatory and Skin Protective Effects ofJournal of microbiology and biotechnology · 2024Article
- Phytochemical Content, Antibacterial Activity, and Antioxidant, Anti-Inflammatory, and Cytotoxic Effects of Traditional Medicinal Plants against Respiratory Tract Bacterial Pathogens.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- CD38: An Immunomodulatory Molecule in Inflammation and Autoimmunity.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Inflammation is a process driven by underlying cell-cell communication and many other factors. In this study, a model of cell-cell communications was proposed to study factors driving the inflammation time course. Analyses of inflammations that are driven by the combined effects of strain (mechanical stimuli) and/or pathogens are considered in this paper. An agent-based model was employed to simulate inflammation where macrophages and fibroblasts influence each other through cell signaling cytokines that diffuse and spread in the tissue space. The communication network of macrophages and fibroblasts was then inferred and its network model (termed TE network) was generated and analyzed. The results suggest that factors driving inflammation time course can be discriminated by the characteristics of TE networks. Inflammation driven only by pathogens has certain TE network characteristics indicating slower and lower information exchange among cells. Multiple stimuli can help to maintain sufficient information exchange among cells, which is beneficial for inflammation resolution. The TE network captures the unfolding of the innate immune system over time, and the history of pathogens invasion. The resulting network leads to an improved understanding of the resilience of the system to future pathogen invasion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.