Evidence map›Paper›PMID 39002011›Full record

ArticleDoklady. Biochemistry and biophysics2024

Proinflammatory Activation of Monocytes in Patients with Immunoinflammatory Rheumatic Diseases.

A I Bogatyreva, E V Gerasimova, T V Kirichenko, Yu V Markina, T V Popkova, M V Shalygina, T V Tolstik, A M Markin, A N Orekhov

Abstract read
PubMed Publisher
In one paragraph

Article in Doklady. Biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. [Causal relationship between circulating cytokines and keloids: A Mendelian randomized study].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  2. Article
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

9 authors.

A I BogatyrevaAvtsyn Research Institute of Human Morphology, Petrovsky Russian Scientific Center of Surgery, Moscow, Russia.
E V GerasimovaNasonova Research Institute of Rheumatology, Moscow, Russia. gerasimovaev@list.ru.
T V KirichenkoAvtsyn Research Institute of Human Morphology, Petrovsky Russian Scientific Center of Surgery, Moscow, Russia.
Yu V MarkinaAvtsyn Research Institute of Human Morphology, Petrovsky Russian Scientific Center of Surgery, Moscow, Russia.
T V PopkovaNasonova Research Institute of Rheumatology, Moscow, Russia.
M V ShalyginaNasonova Research Institute of Rheumatology, Moscow, Russia.
T V TolstikAvtsyn Research Institute of Human Morphology, Petrovsky Russian Scientific Center of Surgery, Moscow, Russia.
A M MarkinAvtsyn Research Institute of Human Morphology, Petrovsky Russian Scientific Center of Surgery, Moscow, Russia.
A N OrekhovAvtsyn Research Institute of Human Morphology, Petrovsky Russian Scientific Center of Surgery, Moscow, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of immunoinflammatory rheumatic diseases (IRDs) is based on chronic inflammation, one of the key mechanisms of which may be abnormal activation of macrophages, leading to further disruption of the immune system.

objective. The objective of this study was to evaluate the proinflammatory activation of circulating monocytes in patients with IRDs. MATERIALS AND

methods. The study involved 149 participants (53 patients with rheumatoid arthritis (RA), 45 patients with systemic lupus erythematosus (SLE), 34 patients with systemic scleroderma (SSc), and 17 participants without IRDs) 30 to 65 years old. Basal and lipopolysaccharide (LPS)-stimulated secretion of monocytes was studied in a primary culture of monocytes obtained from blood by immunomagnetic separation. Quantitative assessment of the cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), as well as the chemokine monocyte chemoattractant protein-1 (MCP-1) was carried out in the culture fluid by ELISA. Proinflammatory activation of monocytes was calculated as the ratio of LPS-stimulated and basal secretions.

results. It was shown that the basal secretion of all studied cytokines was significantly increased in all groups of patients with IRDs, except for the secretion of IL-1β in the SLE group, compared to the control. LPS-stimulated secretion of TNF-α was increased and MCP-1 was decreased in patients with IRDs compared to the control group; LPS-stimulated IL-1β secretion only in the SSc group significantly differed from the control group. In the RA group, monocyte activation was reduced for all cytokines compared to the control; in the SLE group, for TNF-α and MCP-1; in the SSc group, for MCP-1.

conclusions. The decrease in proinflammatory activation of monocytes in patients with IRDs is due to a high level of basal secretion of cytokines, which can lead to disruption of the adequate immune response in these diseases and is an important link in the pathogenesis of chronic inflammation.

Indexed as

InflammationMonocytesAdultAgedArthritis, RheumatoidChemokine CCL2CytokinesFemaleHumansInterleukin-1betaLipopolysaccharidesLupus Erythematosus, SystemicMaleMiddle AgedRheumatic DiseasesScleroderma, SystemicChemokine CCL2CytokinesInterleukin-1betaLipopolysaccharidesTumor Necrosis Factor-alphaIL-1βMCP-1monocyte activationproinflammatory cytokinesrheumatoid arthritissystemic lupus erythematosussystemic sclerodermaTNF-α

Identifiers

PMID39002011

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.