Evidence map›Paper›PMID 42609017›Full record

ArticleEuropean journal of immunology2026

Monocytes Display Altered Inflammatory Profiles in Individuals with Diabetic Foot Ulcers Indicating Monocyte Dysfunction.

Rekha Marimuthu, Heather J Medbury, Rana Baraz, Mauro Vicaretti, Sue-Lynn Lau, Jenny E Gunton, Stephen Li, Helen Williams

Abstract read
In one paragraph

Article in European journal of immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Rekha MarimuthuDepartment of Surgery, Vascular Biology Research Centre, Westmead Hospital, Westmead, Australia.
Heather J MedburyDepartment of Surgery, Vascular Biology Research Centre, Westmead Hospital, Westmead, Australia.
Rana BarazDepartment of Surgery, Vascular Biology Research Centre, Westmead Hospital, Westmead, Australia.
Mauro VicarettiDepartment of Surgery, Vascular Biology Research Centre, Westmead Hospital, Westmead, Australia.
Sue-Lynn LauSydney Medical School, The University of Sydney, Westmead, Australia.
Jenny E GuntonSydney Medical School, The University of Sydney, Westmead, Australia.
Stephen LiDepartment of Surgery, Vascular Biology Research Centre, Westmead Hospital, Westmead, Australia.
Helen WilliamsDepartment of Surgery, Vascular Biology Research Centre, Westmead Hospital, Westmead, Australia.

Funding

NSWHP-ICMPR-Westmead Private Practice Fund and Westmead Hospital-WSLHD, NSW HealthWestmead Research Hub, the Cancer Institute New South Wales, the National Health and Medical Research Council and the Ian Potter Foundation
6 · The paper itself

Abstract

Diabetic foot ulcers (DFUs) often exhibit impaired healing. Macrophage imbalance driven by persistent inflammation is one contributing factor, with a predominance of inflammatory over anti-inflammatory macrophages in non-healing ulcers. Monocytes, precursors of macrophages, are skewed towards an inflammatory phenotype in diabetes. Here, we investigated whether monocyte inflammatory skewing is further exacerbated in individuals with DFUs and explored how it relates to an individual's metabolic (HbA1c and lipids) profile. Monocyte inflammatory profile was assessed by examining phenotypic markers, gene expression, and cytokine production. We observed an elevation in total monocytes and the intermediate subset in the DFU group compared with healthy individuals. In addition, an impaired monocyte profile was seen in the DFU group, with a suppression of both inflammatory (CD86, TLR2, and TLR4) and anti-inflammatory (CD163) markers, accompanied by the downregulation of distinct inflammatory and anti-inflammatory genes. Despite a suppressed phenotype, DFU monocytes showed an increased basal TNF and IFN-γ production, indicating low-grade inflammation. Further, in exploratory analysis, monocyte CD86 and CD163 inversely correlated with HbA1c, while CD163 negatively correlated with cholesterol/HDL-C and triglycerides, suggesting links between metabolic control and monocyte phenotype. Taken together, the impaired monocyte profile indicates underlying pathogenic inflammation and monocyte dysfunction in people with DFUs, suggesting the monocyte profile could serve as a potential biomarker for immunomodulation in DFU.

Indexed as

Diabetic FootInflammationMonocytesAdultAgedAntigens, CDAntigens, Differentiation, MyelomonocyticB7-2 AntigenBiomarkersCD163 AntigenFemaleGlycated HemoglobinHumansMacrophagesMaleMiddle AgedAntigens, CDAntigens, Differentiation, MyelomonocyticB7-2 AntigenBiomarkersCD163 AntigenCD86 protein, humanGlycated Hemoglobinhemoglobin A1c protein, humanReceptors, Cell SurfaceTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4diabetic foot ulcersinflammationmonocyte dysfunctionmonocytesmonocyte surface markers

Identifiers

PMID42609017
PMCPMC13482121

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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.