ArticleExperimental and therapeutic medicine2014
Role of p38 MAPK and STAT3 in lipopolysaccharide-stimulated mouse alveolar macrophages.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 48 citations in OpenAlex.
- Synthetic mucus biomaterials enable localized therapeutic antibody delivery in inflammatory bowel disease.APL bioengineering · 2026Article
- Cytoarchitectural multi-depot profiling reveals immune-metabolic crosstalk in human colon-associated adipose tissue.Cell metabolism · 2026Article
- Unravelling butyrate metabolism in sepsis: identification of key genes.BMC infectious diseases · 2025Article
- The volatile oil ofFrontiers in pharmacology · 2025Article
- Fisetin modulates the gut microbiota alongside biomarkers of senescence and inflammation in a DSS-induced murine model of colitis.GeroScience · 2024Article
- Engineered extracellular vesicles carrying let-7a-5p for alleviating inflammation in acute lung injury.Journal of biomedical science · 2024Article
- Suppression by central adenosine A3 receptors of the cholinergic defense against cardiovascular aberrations of sepsis: role of PI3K/MAPKs/NFκB signaling.Frontiers in pharmacology · 2024Article
- GRaNIE and GRaNPA: inference and evaluation of enhancer-mediated gene regulatory networks.Molecular systems biology · 2023Article
- Advances in the role of STAT3 in macrophage polarization.Frontiers in immunology · 2023Review
- A deubiquitination module essential for TScience advances · 2022Article
- Anti-neuroinflammatory effects ofHeliyon · 2022Article
- High glucose enhances lipopolysaccharide-induced inflammation in cultured BV2 microglial cell line.Immunity, inflammation and disease · 2022Article
- TIRAP-mediated activation of p38 MAPK in inflammatory signaling.Scientific reports · 2022Article
- A pregnancy hormone-cell death link promotes enhanced lupus-specific immunological effects.Frontiers in immunology · 2022Article
- Corylin Ameliorates LPS-Induced Acute Lung Injury via Suppressing the MAPKs and IL-6/STAT3 Signaling Pathways.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Cystatin C Deficiency Increases LPS-Induced Sepsis and NLRP3 Inflammasome Activation in Mice.Cells · 2021Article
- The Dynamic Role of Microglia and the Endocannabinoid System in Neuroinflammation.Frontiers in pharmacology · 2021Review
- Biochanin A impedes STAT3 activation by upregulating p38δ MAPK phosphorylation in IL-6-stimulated macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Beneficial effect of STAT3 decoy oligodeoxynucleotide transfection on organ injury and mortality in mice with cecal ligation and puncture-induced sepsis.Scientific reports · 2020Article
- Changes in H3K27ac at Gene Regulatory Regions in Porcine Alveolar Macrophages Following LPS or PolyIC Exposure.Frontiers in genetics · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive production of inflammatory mediators is an important feature of inflammatory lung disease. In macrophages, mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) are crucial mediators for the production of proinflammatory cytokines. In the present study, the role of MAPK and STAT3 on tumor necrosis factor (TNF)-α and interleukin (IL)-10 production was investigated in mouse alveolar macrophages. The levels of TNF-α and IL-10 in lipopolysaccharide (LPS; 100 ng/ml)-stimulated MH-S cell lines were measured by an enzyme-linked immunosorbent assay, with or without p38 inhibitor (SB203580; 5, 10 or 15 μM) intervention. Phosphorylated STAT3 (p-STAT3) expression was examined by western blot analysis and immunocytochemistry following LPS stimulation for 15 or 30 min. Antibodies against STAT3 were used to verify comparable sample loading. Cells stimulated with LPS showed significantly increased levels of p-STAT3 protein (P<0.05) when compared with the baseline levels. TNF-α and IL-10 protein levels also increased following LPS stimulation (P<0.05). By contrast, treatment with the p38 inhibitor, SB203580, decreased the levels of p-STAT3, TNF-α and IL-10 (P<0.05) following LPS stimulation. SB203580 was shown to inhibit LPS-stimulated TNF-α expression (P<0.05) in a concentration-dependent manner, reaching significance at a concentration of 10 μM. However, the inhibition of IL-10 expression was not concentration-dependent. Therefore, LPS-stimulated overproduction of TNF-α and IL-10 is mediated at least partially by the MAPK pathway. Inhibition of p38 prevented LPS-induced STAT3 phosphorylation, indicating an interaction between the STAT3 and MAPK signaling pathways.
Indexed as
Identifiers
What Socratic 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 Socratic graph.