ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
objectiveTuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a significant global health burden, characterized by complex host-pathogen interactions that drive heterogeneous clinical outcomes. While pulmonary epithelial cells are increasingly recognized as active participants in innate immunity during Mtb infection, how host defense are altered when the epithelial barrier is compromised remains unclear.
methodsIn this study, we developed a murine model combining naphthalene-induced pulmonary epithelial injury with Mtb infection and mapped the pulmonary cells landscape through single-cell RNA sequencing (scRNA-seq), followed by in vitro stimulation assays to validate macrophage functional changes.
resultsNotably, we found a pronounced impairment in pulmonary bacterial clearance. Transcriptomic analysis revealed a widespread suppression of epithelial immune functions and showed that macrophages transitioned from an antimicrobial to an antigen-presenting phenotype, indicating waning pulmonary innate defenses and heightened adaptive immune activation. In vitro experiments further suggested that this macrophage transition may be linked to epithelial cell alterations.
conclusionsThese findings indicate that pulmonary epithelial integrity may influence early host immune responses to Mycobacterium tuberculosis and provide a transcriptomic framework for exploring epithelial-immune crosstalk as a potential therapeutic target.
Indexed as
Identifiers
What Socratic 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 Socratic graph.