ArticleFrontiers in immunology2026
Alpha7 nicotinic acetylcholine receptor activation attenuates allergic airway inflammation and is associated with heme oxygenase-1 induction.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Activation of the α7 nicotinic acetylcholine receptor (α7nAChR) exerts anti-inflammatory effects; however, its role in allergic airway inflammation remains poorly understood. This study investigated how GTS-21 treatment, consistent with α7nAChR activation, influences airway inflammation and epithelial cytokine responses. Methods: A murine model of allergic airway inflammation was established in female C57BL/6J mice by repeated house dust mite (HDM) exposure. Mice received intratracheal GTS-21 or phosphate-buffered saline (PBS) prior to each HDM challenge. Airway inflammation and cytokine levels were then evaluated. Results: Intratracheal GTS-21 administration significantly attenuated HDM-induced eosinophilic airway inflammation in mice and reduced TSLP and type 2 cytokine levels. In BEAS-2B cells, GTS-21 treatment similarly suppressed LPS- and HDM-induced TSLP production. RNA sequencing revealed that GTS-21 treatment upregulated heme oxygenase-1 (HO-1) expression. Increased HO-1 expression was associated with reduced TSLP production under these experimental conditions. Conclusion: GTS-21 attenuated allergic airway inflammation and suppressed epithelial TSLP production in association with increased HO-1 expression. These findings suggest that cholinergic receptor-associated signaling may modulate epithelial inflammatory responses in allergic airway inflammation.
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.