ArticleImmunology2018
Inhaled Cryptococcus neoformans elicits allergic airway inflammation independent of Nuclear Factor Kappa B signalling in lung epithelial cells.
Article in Immunology, 2018. 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.
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- Pulmonary Fibrosis and Hypereosinophilia in TLR9Pathogens (Basel, Switzerland) · 2022Article
- Anti-inflammatory actions of aspirin-triggered resolvin D1 (AT-RvD1) in bronchial epithelial cells infected with Cryptococcus neoformans.Inflammopharmacology · 2021Article
- Infectious particle identity determines dissemination and disease outcome for the inhaled human fungal pathogen Cryptococcus.PLoS pathogens · 2019Article
- Helper T-cell responses and pulmonary fungal infections.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
5 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary challenge with the ubiquitous fungus Cryptococcus neoformans results in allergic airway inflammation (AAI) characterized by robust recruitment of eosinophils and T cells producing type 2 cytokines to the lungs. Previous studies have demonstrated a critical role for Nuclear Factor Kappa B (NF-κB) activation within lung epithelial cells (LECs) in driving AAI in response to protein allergens, yet the role of LEC-intrinsic NF-κB in promoting AAI following exposure to C. neoformans is poorly understood. To investigate the role of LEC-intrinsic NF-κB in promoting AAI following C. neoformans challenge, we used IKK
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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.