ArticleFrontiers in pharmacology2025
Carnosine as a protective metabolic mediator in inflammatory lung injury by inhibiting macrophage infiltration and M1-like polarization.
Article in Frontiers in pharmacology, 2025. 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Inflammatory lung injury is a common pathological feature of pneumonia caused by various infectious and non-infectious agents. However, metabolic regulators that can mitigate inflammation and immune cell infiltration in diverse lung injury models remain poorly understood. Methods: Using targeted metabolomic profiling of lung tissues collected on day 5 from two distinct murine models of lung inflammation-lipopolysaccharide (LPS)-induced and papain-induced-we identified carnosine as a commonly downregulated metabolite in both models. To evaluate its therapeutic potential, we administered exogenous carnosine in both models and assessed its effects on body weight, inflammatory cytokine expression, and histopathological changes. Results: Carnosine supplementation significantly improved body weight maintenance, reduced the expression of pro-inflammatory cytokines, and attenuated histological lung damage in both LPS- and papain-induced lung injury models. Flow cytometry analysis revealed that carnosine treatment markedly decreased pulmonary infiltration of macrophages and neutrophils. Multiplex immunofluorescence further demonstrated a significant reduction of macrophage accumulation in the peribronchial regions of the lung following carnosine administration. In vitro experiments using bone marrow-derived macrophages (BMDMs) confirmed that carnosine effectively suppressed LPS-induced inflammatory responses and inhibited polarization toward the M1-like macrophage phenotype. Conclusion: Our findings identify carnosine as a protective metabolic mediator in inflammatory lung injury and demonstrate its capacity to alleviate pulmonary inflammation by modulating innate immune cell recruitment and macrophage polarization. These results highlight the translational potential of carnosine as a therapeutic agent for treating inflammatory lung diseases.
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.