What markers track resolution of inflammation?
Resolution of inflammation is an active process with measurable markers. This page surveys research on follistatin, specialized pro-resolving mediators, doxycycline, and other agents, and the markers used to track their
What markers track resolution of inflammation?
Resolution of inflammation is an active, coordinated process driven by endogenous mediators and is tracked in research by markers such as specialized pro-resolving mediators (SPMs), matrix metalloproteinase (MMP) activity relative to tissue inhibitors of metalloproteinases (TIMPs), aortic lesion area, and plasma lipid profiles. These markers are used across models ranging from murine atherosclerosis to human clinical trials.
Follistatin (FST) is a secreted glycoprotein that binds and neutralizes members of the transforming growth factor-beta (TGF-β) superfamily, regulating skeletal muscle, adipose, and bone homeostasis [1]. The work described here centres on TGF-β superfamily signalling and its downstream effects on arginine metabolism and adipose browning [1].
Research Studies
Follistatin and atherosclerosis in the Hybrid Mouse Diversity Panel
Transcriptomic and metabolomic analyses of the Hybrid Mouse Diversity Panel (HMDP) revealed that Fst expression was negatively correlated with aortic lesion area [1]. In mice, FST promotes adipose browning and enhances energy metabolism, leading to improved plasma lipid profiles and metabolic health [1]. Given the association between brown adipose tissue (BAT) activation and reduced atherosclerosis, investigators tested the anti-atherogenic potential of FST [1]. The study reported that FST mitigates atherosclerosis through activation of arginine metabolism and adipose browning [1]. These findings are animal-only.
Oral SPM supplementation and vascular ageing in obese hypertensive patients
A clinical trial is investigating the effect of oral SPM supplementation on inflammation-induced vascular ageing in obese hypertensive patients [2]. The rationale notes that cardiovascular risk factors such as obesity, diabetes, high blood pressure, high cholesterol, or smoking increase the risk of myocardial infarction, stroke, or peripheral artery disease, and that even with optimal treatment, high-risk individuals face residual cardiovascular risk attributed to inflammation-driven vascular lesions [2]. This trial is in a human population.
Adjunctive doxycycline for central nervous system tuberculosis
In central nervous system tuberculosis (CNS-TB), the activity of pathogenic host matrix metalloproteinases (MMPs) is unopposed to tissue inhibitors of metalloproteinases (TIMPs), resulting in a matrix-degrading phenotype that may drive worse outcomes [3]. In a prior established CNS-TB murine model, investigators demonstrated that adjunctive MMP inhibition using doxycycline [3]. The current study evaluates adjunctive doxycycline for CNS-TB [3]. This work includes animal-model evidence and a human trial.
Doxycycline host-directed therapy in pulmonary tuberculosis
A recent Phase 2b double-blind randomised-controlled clinical trial showed that adjunctive doxycycline therapy is safe, accelerates resolution of inflammation, suppresses tissue damaging enzyme activity and decreases pulmonary cavity volume [4]. A Phase III trial aims to determine if adjunctive doxycycline can reduce pulmonary impairment after tuberculosis (PIAT) and improve cardiovascular outcomes in a fully powered trial of 8 weeks of adjunctive doxycycline alongside standard pulmonary TB treatment [4]. This is human clinical trial evidence.
Dental pulp stem cells and plaque biofilm-associated infections
A structured narrative review synthesised evidence from 2000–2025 on the antimicrobial, immunomodulatory, and regenerative properties of dental pulp stem cells (DPSCs) in the context of plaque-induced gingivitis and oral biofilm infections [5]. This is a review of in vitro and clinical literature.
Recombinant Klotho protein and sterile inflammation after hemorrhagic shock
Hemorrhagic shock is characterised by systemic hypoperfusion, which induces inflammatory responses, oxidative stress, and apoptosis, often leading to multiple organ failure [6]. Klotho, an antiaging protein with anti-inflammatory, antiapoptotic, and antioxidative properties, has been studied for its protective effects [6]. This is animal-model evidence.
Markers compared across studies
| Marker | Context | Evidence type |
|---|---|---|
| Aortic lesion area | Follistatin in HMDP mice [1] | Animal |
| Plasma lipid profiles | Follistatin in mice [1] | Animal |
| MMP/TIMP balance | CNS-TB murine model [3] | Animal |
| Pulmonary cavity volume | Adjunctive doxycycline in TB [4] | Human |
| Resolution of inflammation | Adjunctive doxycycline in TB [4] | Human |
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Sources
- [1] Follistatin Mitigates Atherosclerosis Through Activation of Arginine Metabolism and Adipose Browning
- [2] The Effect of Oral SPM Supplementation on INflammation-induced Vascular Ageing in Obese Hypertensive Patients
- [3] Adjunctive Doxycycline for Central Nervous System Tuberculosis
- [4] Doxycycline Host-directed Therapy to Improve Lung Function and Decrease Tissue Destruction in Pulmonary Tuberculosis
- [5] Dental Pulp Stem Cells for the Management of Plaque Biofilm-Associated Infections : A Review.
- [6] Recombinant Klotho Protein Protects Tissues by Mitigating the Detrimental Effects of Sterile Inflammation After Hemorrhagic Shock.