ArticleLung2015
An Adenoviral Vector Encoding Full-Length Dectin-1 Promotes Aspergillus-Induced Innate Immune Response in Macrophages.
Article in Lung, 2015. 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
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Spatiotemporal modeling quantifies cellular contributions to uptake of Aspergillus fumigatus in the human lung.Communications biology · 2024Article
- Article
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- PU.1 serves a critical role in the innate defense against Aspergillus fumigatus via dendritic cell-associated C-type lectin receptor-1 and toll-like receptors-2 and 4 in THP-1-derived macrophages.Molecular medicine reports · 2017Article
- Up-regulation of Dectin-1 in airway epithelial cells promotes mice defense against invasive pulmonary aspergillosis.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe incidence of invasive pulmonary aspergillosis (IPA) has increased significantly over the last two decades. Alveolar macrophages (AMs) represent the first line of pulmonary host response to Aspergillus conidia. Recognition of conidia by AMs involves Dectin-1 (CLEC7A), which is a conserved structure to combine β-glucans. The deficiency of Dectin-1 results in impaired fungal killing and uncontrolled growth of Aspergillus fumigatus. Thus, we hypothesized that high expression of Dectin-1 would enhance the host recognition and fungal killing.
methodsWe set out to develop an adenoviral vector encoding full-length Dectin-1 (Ad-Dectin-1-EGFP) and then transfect it to MH-S cells. Transfect cell model was verified by using real-time RT-PCR, Western blot, flow cytometric, and confocal microscopic assays. And also, the function of Dectin-1 was explored by measuring cytokine release and killing ability during the course of A. fumigatus infection.
resultsWe constructed a recombinant adenovirus which could upregulate the expression of Dectin-1 and verified that Dectin-1 was expressed on cell membrane. The function of Dectin-1 was also demonstrated by its ability in promoting the production of cytokines and increasing the killing ability during the course of A. fumigatus infection.
conclusionsAn adenoviral vector was successfully applied to the production of a recombinant adenovirus encoding full-length Dectin-1, and also, its function in Aspergillus-induced innate immune response was demonstrated.
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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.