ArticleMolecular medicine reports2017
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.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Review
- Efficacy of voriconazole combined with caspofungin in treating Chronic Obstructive Pulmonary Disease patients with invasive pulmonary aspergillosis: impacts on clinical outcomes, inflammatory cytokines, and immune markers.Frontiers in immunology · 2026Article
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- Andrographolide Attenuates NLRP3 Inflammasome Activation and Airway Inflammation in Exacerbation of Chronic Obstructive Pulmonary Disease.Drug design, development and therapy · 2024Article
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- Epigallocatechin gallate regulates the myeloid-specific transcription factor PU.1 in macrophages.PloS one · 2024Article
- Survival Factor A (SvfA) Contributes toJournal of fungi (Basel, Switzerland) · 2023Article
- PU.1-CD23 signaling mediates pulmonary innate immunity against Aspergillus fumigatus infection by driving inflammatory response.BMC immunology · 2023Article
- Alcohol impairs recognition and uptake of Mycobacterium tuberculosis by suppressing toll-like receptor 2 expression.Alcoholism, clinical and experimental research · 2022Article
- Human Corneal Epithelial Cells Internalize Aspergillus flavus Spores by Actin-Mediated Endocytosis.Infection and immunity · 2021Article
- The Pathogenesis ofPolish journal of microbiology · 2021Review
- Article
- Deficiency of GPI Glycan Modification by Ethanolamine Phosphate Results in Increased Adhesion and Immune Resistance ofFrontiers in cellular and infection microbiology · 2021Article
- The mechanisms of hydroxychloroquine in rheumatoid arthritis treatment: Inhibition of dendritic cell functions via Toll like receptor 9 signaling.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- Human and Murine Innate Immune Cell Populations Display Common and Distinct Response Patterns during TheirFrontiers in immunology · 2017Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aspergillus fumigatus (A. fumigatus) is one of the most common fungal pathogens of invasive pulmonary aspergillosis (IPA), which may be life threatening in immunocompromised individuals. The dendritic cell-associated C-type lectin receptor (Dectin-1), toll‑like receptor (TLR)-2 and TLR-4 are major pattern recognition receptors in alveolar macrophages that recognize A. fumigatus components. The PU.1 transcription factor is known to be important for the transcriptional control of these three receptors in mature macrophages. The present study investigated whether alterations of PU.1 expression may affect the innate defense against A. fumigatus in the human monocyte THP‑1 cell line. THP-1-derived macrophages were transduced with PU.1 adenoviral vectors and transfected with PU.1 small interfering RNA, and the mRNA and protein expression levels of Dectin‑1, TLR‑2 and TLR‑4 were measured. In addition, the levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β were ascertained, and fungal phagocytosis and killing were assessed. The results demonstrated that overexpression of PU.1 by recombinant adenoviral vectors resulted in a significant upregulation of Dectin‑1, TLR‑2 and TLR‑4 at the transcriptional and translational levels. In response to A. fumigatus stimulation, PU.1 overexpression increased TNF‑α and IL‑1β production. In addition, Dectin‑1, TLR‑2 and TLR‑4 upregulation may have enhanced the phagocytosis and killing ability of THP‑1‑derived macrophages. As expected, silencing of PU.1 led to downregulation of Dectin‑1, TLR‑2, TLR‑4 and the expression of pro‑inflammatory cytokines, as well as decreased phagocytosis and the killing ability of THP1‑derived macrophages. In conclusion, the results indicate that PU.1 may be a critical factor for the innate defense against A. fumigatus, and may therefore be a potential target for the prophylaxis and treatment of IPA.
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