Evidence map›Paper›PMID 35647912›Full record

ArticleClinical and experimental immunology2022

Increased TNF-α production in response to IL-6 in patients with systemic inflammation without infection.

Graciela L Cabrera-Rivera, Ruth L Madera-Sandoval, José Israel León-Pedroza, Eduardo Ferat-Osorio, Enrique Salazar-Rios, Juan A Hernández-Aceves, Uriel Guadarrama-Aranda, Constantino López-Macías, Isabel Wong-Baeza, Lourdes A Arriaga-Pizano

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 8% of its field
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

37 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  4. Observational
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  9. Prognostic role of systemic inflammatory indices in predicting the severity of acute calculous cholecystitis.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2026
    Article
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  14. Neuroimmune cross-talk inFrontiers in immunology · 2026
    Review
  15. Article
  16. Review
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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

10 authors at 3 institutions in 2 countries.

Graciela L Cabrera-RiveraUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.ORCID 0000-0002-1107-0958
Ruth L Madera-SandovalUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
José Israel León-PedrozaCoordinación de Investigación, Unidad 401-C, Urgencias Médicas, Hospital General de México "Dr. Eduardo Liceaga", Mexico City, Mexico.
Eduardo Ferat-OsorioUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Enrique Salazar-RiosUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.ORCID 0000-0002-0054-322X
Juan A Hernández-AcevesUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Uriel Guadarrama-ArandaUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Constantino López-MacíasUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Isabel Wong-BaezaDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico.
Lourdes A Arriaga-PizanoUnidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Mexican Social Security Institute · MXHospital General de México · MXInstituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute systemic inflammation can lead to life-threatening organ dysfunction. In patients with sepsis, systemic inflammation is triggered in response to infection, but in other patients, a systemic inflammatory response syndrome (SIRS) is triggered by non-infectious events. IL-6 is a major mediator of inflammation, including systemic inflammatory responses. In homeostatic conditions, when IL-6 engages its membrane-bound receptor on myeloid cells, it promotes pro-inflammatory cytokine production, phagocytosis, and cell migration. However, under non-physiologic conditions, such as SIRS and sepsis, leucocyte dysfunction could modify the response of these cells to IL-6. So, our aim was to evaluate the response to IL-6 of monocytes from patients diagnosed with SIRS or sepsis. We observed that monocytes from patients with SIRS, but not from patients with sepsis, produced significantly more TNF-α than monocytes from healthy volunteers, after stimulation with IL-6. Monocytes from SIRS patients had a significantly increased baseline phosphorylation of the p65 subunit of NF-κB, with no differences in STAT3 phosphorylation or SOCS3 levels, compared with monocytes from septic patients, and this increased phosphorylation was maintained during the IL-6 activation. We found no significant differences in the expression levels of the membrane-bound IL-6 receptor, or the serum levels of IL-6, soluble IL-6 receptor, or soluble gp130, between patients with SIRS and patients with sepsis. Our results suggest that, during systemic inflammation in the absence of infection, IL-6 promotes TNF-α production by activating NF-κB, and not the canonical STAT3 pathway.

Indexed as

Interleukin-6SepsisSystemic Inflammatory Response SyndromeTumor Necrosis Factor-alphaHumansInflammationMonocytesNF-kappa BReceptors, Interleukin-6Interleukin-6NF-kappa BReceptors, Interleukin-6Tumor Necrosis Factor-alphamIL-6RNF-κB p-p65sepsissIL-6Rsystemic inflammatory response syndrome

Identifiers

PMID35647912
PMCPMC9390847
OpenAlexW4281684032

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.