ArticleThe Journal of biological chemistry2016
Modulation of Macrophage Inflammatory Nuclear Factor κB (NF-κB) Signaling by Intracellular Cryptococcus neoformans.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 39 citations in OpenAlex.
- Two Methods of Measuring Cryptococcus neoformans Fungal Burden in Macrophages.Methods in molecular biology (Clifton, N.J.) · 2024Article
- "Under Pressure" - How fungi evade, exploit, and modulate cells of the innate immune system.Seminars in immunology · 2023Review
- Article
- Article
- Cryptococcus neoformansmBio · 2021Article
- Cryptococcus neoformans Coinfection Dampens the TNF-α Response in HIV-1-Infected Human THP-1 Macrophages.mSphere · 2021Article
- Article
- Glucose metabolism involved in PD-L1-mediated immune escape in the malignant kidney tumour microenvironment.Cell death discovery · 2021Article
- Anti-Inflammatory Effects of Antarctic LichenBioMed research international · 2021Article
- microRNA-15a-5p participates in sepsis by regulating the inflammatory response of macrophages and targeting TNIP2.Experimental and therapeutic medicine · 2020Article
- Intracellular Cryptococcus neoformans disrupts the transcriptome profile of M1- and M2-polarized host macrophages.PloS one · 2020Article
- Clinical significance and prospective molecular mechanism of C‑C motif chemokine receptors in patients with early‑stage pancreatic ductal adenocarcinoma after pancreaticoduodenectomy.Oncology reports · 2019Article
- Polyphenol mixture of a native Korean variety of Artemisia argyi H. (Seomae mugwort) and its anti‑inflammatory effects.International journal of molecular medicine · 2019Article
- O-GlcNAcylation in immunity and inflammation: An intricate system (Review).International journal of molecular medicine · 2019Review
- Long noncoding RNA expression profile from cryptococcal meningitis patients identifies DPY19L1p1 as a new disease marker.CNS neuroscience & therapeutics · 2019Article
- Lipopolysaccharide-Induced Increase in Intestinal Permeability Is Mediated by TAK-1 Activation of IKK and MLCK/MYLK Gene.The American journal of pathology · 2019Article
- MicroRNA-181a-5p Regulates Inflammatory Response of Macrophages in Sepsis.Open medicine (Warsaw, Poland) · 2019Article
- CNS infection and immune privilege.Nature reviews. Neuroscience · 2018Review
- A Predicted Mannoprotein Participates inmSphere · 2018Article
- Innate Immunity against Cryptococcus, from Recognition to Elimination.Journal of fungi (Basel, Switzerland) · 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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cryptococcus neoformans (Cn) is a common facultative intracellular pathogen that can cause life-threatening fungal meningitis in immunocompromised individuals. Shortly after infection, Cn is detectable as both extra- and intracellular yeast particles, with Cn being capable of establishing long-lasting latent infections within host macrophages. Although recent studies have shown that shed capsular polysaccharides and intact extracellular Cn can compromise macrophage function through modulation of NF-κB signaling, it is currently unclear whether intracellular Cn also affects NF-κB signaling. Utilizing live cell imaging and computational modeling, we find that extra- and intracellular Cn support distinct modes of NF-κB signaling in cultured murine macrophages. Specifically, in RAW 264.7 murine macrophages treated with extracellular glucuronoxylomannan (GXM), the major Cn capsular polysaccharide, LPS-induced nuclear translocation of p65 is inhibited, whereas in cells with intracellular Cn, LPS-induced nuclear translocation of p65 is both amplified and sustained. Mathematical simulations and quantification of nascent protein expression indicate that this is a possible consequence of Cn-induced "translational interference," impeding IκBα resynthesis. We also show that long term Cn infection induces stable nuclear localization of p65 and IκBα proteins in the absence of additional pro-inflammatory stimuli. In this case, nuclear localization of p65 is not accompanied by TNFα or inducible NOS (iNOS) expression. These results demonstrate that capsular polysaccharides and intact intracellular yeast manipulate NF-κB via multiple distinct mechanisms and provide new insights into how Cn might modulate cellular signaling at different stages of an infection.
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.