Evidence map›Paper›PMID 39847177›Full record

ArticleBulletin of mathematical biology2025

Modeling Innate Immunity Causing Chronic Inflammation and Tissue Damage.

Kosei Matsuo, Yoh Iwasa

Abstract read
In one paragraph

Article in Bulletin of mathematical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Kosei MatsuoDepartment of Biology, Faculty of Science, Kyushu University, 744 Motooka, Nishi-Ku, Fukuoka, 819-0395, Japan.
Yoh IwasaDepartment of Biology, Faculty of Science, Kyushu University, 744 Motooka, Nishi-Ku, Fukuoka, 819-0395, Japan. yohiwasa@kyudai.jp.ORCID http://orcid.org/0000-0003-0691-1852

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mathematical models of immune responses have traditionally focused on adaptive immunity and pathogen-immune dynamics. However, recent advances in immunology have highlighted the critical role of innate immunity. In response to physical damage or pathogen attacks, innate immune cells circulating throughout the body rapidly migrate from blood vessels and accumulate at the site of injury, triggering inflammation. These cells engulf, break down, and eliminate pathogens. This innate immune response occurs much faster than adaptive immune responses, which require time for cell activation and proliferation. While inflammation helps eliminate pathogens, it can sometimes lead to chronic inflammation by triggering excessive immune responses, ultimately causing tissue damage. In this study, we examine a simple dynamical model of innate immunity. The analysis indicates that when an infection occurs, it triggers inflammation, which activates the innate immune system and initiates the activation cycle. Consequently, pathogens may be eradicated, leaving behind persistent chronic inflammation. Alternatively, the pathogens may not be eradicated, with their abundance either stabilizing at a positive level or oscillating indefinitely. The dynamics exhibit both transcritical and Hopf bifurcations. When innate immunity is activated in the absence of inflammation, pathogens are eradicated more easily, and the likelihood of oscillations in inflammation, immune responses, and pathogen abundance is reduced.

Indexed as

Immunity, InnateInflammationModels, ImmunologicalAnimalsChronic DiseaseHost-Pathogen InteractionsHumansMathematical ConceptsChronic inflammationNon-inflammatory immune activationPathogen infectionPerpetual oscillationTissue damage

Identifiers

PMID39847177
PMCPMC11760608

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Registered trials

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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.