ArticleBMC infectious diseases2016
PU.1 is involved in the immune response to Aspergillus fumigatus through upregulating Dectin-1 expression.
Article in BMC infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 18 citations in OpenAlex.
- HSF1 in macrophages suppressed the progression of asthma via modulating SIRPα/SHP2-Dectin-1/ SYK mediated ROS and inflammatory responses.Scientific reports · 2025Article
- 125I inhibits the progression of cervical cancer by upregulating the HSF1/PU.1/SYK signaling pathway and consequently enhancing the apoptotic response mediated by ROS/USP7/P53.Scientific reports · 2025Article
- PU.1-CD23 signaling mediates pulmonary innate immunity against Aspergillus fumigatus infection by driving inflammatory response.BMC immunology · 2023Article
- Adipocyte-Specific Ablation of PU.1 Promotes Energy Expenditure and Ameliorates Metabolic Syndrome in Aging Mice.Frontiers in aging · 2021Article
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInvasive aspergillosis is a life-threatening disease, and its incidence has increased in the recent past. Dectin-1 recognizes β-glucans and mediates innate immune responses to Aspergillus fumigatus. Transcription factor PU.1 has been the focus of recent research due to its role in inflammation and infection. However, its role in Dectin-1 regulation during A. fumigatus infection remains to be elucidated.
methodsTHP-1 cells were stimulated with A. fumigatus conidia. We then used real-time RT-PCR, Western blot, and immunofluorescence assays to analyze the mRNA and protein levels and cellular distribution, respectively, of Dectin-1 and PU.1 in stimulated THP-1 cells. Additionally, we used the luciferase reporter assays, chromatin immunoprecipitation (ChIP) assays, electrophoretic mobility shift assays (EMSA), and RNA interference experiments to investigate the role of PU.1 in Dectin-1 regulation.
resultsOur results revealed that Dectin-1 mRNA and protein levels as well as the PU.1 protein level were increased in THP-1 cells stimulated with A. fumigatus conidia, while the mRNA expression level did not significantly change between the stimulated and control groups. We also observed that PU.1 translocated into the nucleus in stimulated THP-1 cells. The results of the luciferase reporter assay showed that PU.1 promoted human Dectin-1 (hDectin-1) gene activity. ChIP and EMSA indicated that PU.1 could bind with hDectin-1 gene promoter at three potential transcription factor-binding sites (TFBSs). In addition, knockdown of PU.1 significantly decreased Dectin-1 expression.
conclusionsThis study demonstrated the novel role of PU.1 in the immune response to A. fumigatus through upregulation of Dectin-1 expression and its translocation to the nucleus in A. fumigatus-stimulated THP-1 cells.
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.