ArticleImmunoHorizons2025
Genetic deletion of Alx/Fpr2 differentially regulates pulmonary inflammation in the absence and presence of acute lung injury.
Article in ImmunoHorizons, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Integrated pro-resolving mechanisms: a new dimension for optimizing anti-inflammatory therapy in asthma - a review of impaired inflammation resolution in airway remodeling.Frontiers in immunology · 2026Review
- Spatial proteomics for the analysis of host-pathogen interactions in mice lungs infected withmicroLife · 2026Article
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
Abstract
The inflammation resolution receptor lipoxin A4/formyl peptide receptor 2 (ALX/FPR2) plays a critical role in immune regulation by binding select oxylipins derived from n-6 and n-3 polyunsaturated fatty acids (PUFAs). While ALX/FPR2 is implicated in controlling inflammation initiation and resolution, its specific role in pulmonary inflammatory responses remains unclear. In this study, we investigated how genetic deletion of Alx/Fpr2 controls oxylipin levels, immune cell populations, and inflammatory cytokines under conditions of homeostasis and injury. Alx/Fpr2 knockout (KO) mice exhibited normal food intake and weight gain but showed impaired glucose and lipid metabolism. Targeted lipidomic analyses by liquid chromatography-tandem mass spectrometry revealed elevated pulmonary concentrations of n-6 and n-3 PUFA-derived oxylipins in KO mice compared to controls. Flow cytometry further demonstrated increased lung infiltration of NK cells, monocytes, and lymphoid cells, indicating a proinflammatory state in the absence of injury. Following 24 h of LPS-induced acute lung injury, IL-1β levels were elevated in KO mice, but pulmonary histopathology, immune cell numbers, and oxylipin levels were comparable to those of controls. These results suggested a protective role of ALX/FPR2 upon acute lung injury, which led us to further investigate the role of ALX/FPR2 upon 72 h of lung injury. Indeed, Alx/Fpr2 KO mice showed reduced bronchoalveolar lavage protein concentration and lower levels of IL-6 and TNF-α. Collectively, these findings demonstrate that ALX/FPR2 deficiency promotes basal pulmonary inflammation but protects against prolonged injury-induced inflammation, highlighting the context-dependent role of this receptor in pulmonary 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.