ArticlePloS one2017
Impact of human monocyte and macrophage polarization on NLR expression and NLRP3 inflammasome activation.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 2 of them syntheses that pooled 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.
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
116 citing papers in PubMed, 2 syntheses or guidelines pooled it, 179 citations in OpenAlex.
- Systematic Review of Multi-Omics Approaches to Investigate Toxicological Effects in Macrophages.International journal of molecular sciences · 2020Pooled it
- Effect of tumor microenvironment on pathogenesis of the head and neck squamous cell carcinoma: a systematic review.Molecular cancer · 2019Pooled it
- Targeted inhibition of ATR kinase promotes antitumor immunity in HNSCC through enhanced STING activation and T cell function.Translational oncology · 2026Article
- Induced pluripotent stem cell-derived macrophages enable broad modeling of human inflammasome signaling.Cell reports methods · 2026Article
- Protocol to study inflammasome activation in induced pluripotent stem cell-derived macrophages.STAR protocols · 2026Article
- Urolithin A activates aryl hydrocarbon receptor-NLRP6-mediated pathways in intestinal epithelial cells to modulate mucosal immunity and strengthen gut barrier integrity.Nature communications · 2026Article
- The Role of Interleukin-18 After Spinal Cord Injury: Mechanisms and Therapeutic Potential.Cells · 2026Review
- Macrophage makeover extreme viral edition: mechanisms of immune subversion and therapeutic perspectives.The Journal of general virology · 2026Review
- Macrophage pyroptosis in inflammatory bowel disease: mechanistic insights, pathological roles and treatment strategies.Frontiers in immunology · 2026Review
- Superior inflammatory response and MASH progression inFrontiers in immunology · 2026Article
- Article
- Monocytes/Macrophages and Atherogenesis.International journal of molecular sciences · 2025Review
- Syndrome of undifferentiated recurrent fever (SURF): a multicenter real-world experience from Türkiye.Clinical rheumatology · 2025Observational
- Dexketoprofen enhances NLRP3 activation via ATPase activity after canonical stimuli.Inflammopharmacology · 2025Article
- Gout and NLRP3 Inflammasome Biology.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Review
- Effects of exercise on neuroinflammation in age-related neurodegenerative disorders.European journal of medical research · 2025Review
- Gut Dysbiosis and Probiotic Therapy in Chronic Kidney Disease: A Comprehensive Review.Probiotics and antimicrobial proteins · 2025Review
- Aging and immunity: the age-old tango.Genes & development · 2025Review
- Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Inflammasomes are multiprotein complexes nucleating around an NLR (Nucleotide-binding domain and Leucine-rich Repeat containing protein), which regulate the secretion of the pro-inflammatory interleukin (IL)-1β and IL-18 cytokines. Monocytes and macrophages, the main cells expressing the inflammasome genes, adapt to their surrounding microenvironment by a phenotypic polarization towards a pro-inflammatory M1 phenotype that promotes inflammation or an anti-inflammatory M2 phenotype important for resolution of inflammation. Despite the importance of inflammasomes in health and disease, little is known about inflammasome gene expression in relevant human cells and the impact of monocyte and macrophage polarization in inflammasome gene expression. We examined the expression of several members of the NLR, caspase and cytokine family, and we studied the activation of the well-described NLRP3 inflammasome in an experimental model of polarized human primary monocytes and monocyte-derived macrophages (M1/M2 phenotypes) before and after activation with LPS, a well-characterized microbial pattern used in inflammasome activation studies. Our results show that the differentiation of monocytes to macrophages alters NLR expression. Polarization using IFN-γ (M1 phenotype), induces among the NLRs studied, only the expression of NOD2. One of the key results of our study is that the induction of NLRP3 expression by LPS is inhibited in the presence of IL-4+IL-13 (M2 phenotype) at both mRNA and protein level in monocytes and macrophages. Unlike caspase-3, the expression of inflammasome-related CASP1 (encodes caspase-1) and CASP4 (encodes caspase-4) is up-regulated in M1 but not in M2 cells. Interestingly, the presence of LPS marginally influenced IL18 mRNA expression and secretion, unlike its impact on IL1B. Our data provide the basis for a better understanding of the role of different inflammasomes within a given environment (M1 and M2) in human cells and their impact in the pathophysiology of several important inflammatory disorders.
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.