ArticleAllergy2026
Role for Complement C5 in Eosinophilic Inflammation of Severe Asthma.
Article in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Advances in the treatment of eosinophilic granulomatosis with polyangiitis.Nature reviews. Rheumatology · 2026Review
- Article
- Combining co-expression analysis and machine learning to explore the diagnostic value of complement and coagulation cascade-related genes in asthma and the functional role of SERPINB2.Briefings in functional genomics · 2026Article
- Quantitative Computed Tomographic Clusters in C-BIOPRED Asthma Cohort: Association with Sputum Proteomics.MedComm · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
backgroundWe investigated the role of the complement system, particularly complement C5, in severe asthma defined from an analysis of sputum proteomics. Although there has been evidence of complement activation in asthma, its role in severe asthma remains unclear.
methodSputum protein expression profiles were analyzed from healthy controls and severe asthma patients using data-dependent acquisition mass spectrometry. Weighted correlation network analysis (WGCNA) was used to define the unique modules that were highly correlated with clinical, physiologic, and inflammatory traits. Differential analysis was performed for the complement C5 pathway protein levels and eosinophilic protein expression as influenced by C5. Asthmatic mouse models were used to verify the effect of complement C5 administration and inhibition.
resultsThe WGCNA "brown" module related to the complement system activation was positively correlated with eosinophilic inflammation. Specifically, C5 and downstream complement proteins were up-regulated in patients with high sputum eosinophil levels (≥ 3%) compared to low sputum eosinophils (< 3%). Patients with reduced C5 expression had less eosinophilic inflammation and better lung function. Using single-cell RNA sequencing and immunofluorescence staining led to identification of macrophages as the main source of C5. In vivo experiments confirmed that inhibiting C5 reduced inflammation in allergic mouse models, while direct stimulation with recombinant C5 in IL-5 transgenic mice increased eosinophilic inflammation.
conclusionWe demonstrate a direct role for complement C5 in exacerbating eosinophilic inflammation in severe asthma.
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.