ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2015
TNF-alpha modulates adipose macrophage polarization to M1 phenotype in response to scorpion venom.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- M2 polarization of macrophages: Manipulation of spinal cord injury repair.Neural regeneration research · 2026Article
- Traditional Chinese herbal medicines suppress endometriosis development through modulating macrophage-mediated immune responses in the peritoneal cavity.BioMedicine · 2026Article
- Scorpion Venom as a Source of Cancer Drugs: A Comprehensive Proteomic Analysis and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Proteasome-driven modulation of immune and oxidative pathways during scorpion envenomation pathogenesis.The journal of venomous animals and toxins including tropical diseases · 2025Article
- Network pharmacology-based approach to research the effects and mechanisms ofFrontiers in medicine · 2025Article
- Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.The Japanese dental science review · 2022Review
- Review
- The angiogenic potential of CD271+ human adipose tissue-derived mesenchymal stem cells.Stem cell research & therapy · 2021Article
- Mechanisms of Macrophage Plasticity in the Tumor Environment: Manipulating Activation State to Improve Outcomes.Frontiers in immunology · 2021Review
- The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach.Life sciences · 2020Review
- Differential effect of Androctonus australis hector venom components on macrophage KEuropean biophysics journal : EBJ · 2019Article
- iRhom2-mediated proinflammatory signalling regulates heart repair following myocardial infarction.JCI insight · 2018Article
- CTLA-4 positive breast cancer cells suppress dendritic cells maturation and function.Oncotarget · 2017Article
- F2 peptide fraction ofAvicenna journal of phytomedicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveWe previously reported that Androctonus australis hector (Aah) venom and its toxic fraction affect adipose tissue metabolism. However, the contribution of immune system and the role of adipose tissue macrophages (ATMs) in the progression of inflammation induced by scorpion venom remain largely unknown.
methodsHere we evaluate the capacity of the toxic fraction of Aah venom (FTox-G50) to induce the expression of M1 and M2 markers genes on adipose tissue and isolated stromal vascular cells (SVC). Quantitative real-time PCR was performed on the SVC 24 h after FTox-G50 venom injection to assess the gene expressions of IL12p40, IL23, and other macrophages-associated markers.
resultsWe found that ATM from FTox-G50-venom-injected mice markedly increased the expressions of IL-12p40 and IL-23. Furthermore, the expression of nitric oxide synthase 2 (an M1 marker) was up-regulated, but the expression of Arginase1 (an M2 marker) was not. Systemic injection of a chemical inhibitor directed against TNF-α binding reduced the expression of inflammatory M1 macrophage markers and the MAPKpk2 gene, a key mediator of inflammatory signaling.
conclusionThese results indicate that TNF-α is a physiological regulator of inflammation and macrophage activation induced by scorpion venom.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.