ArticleBMC immunology2025
Chlorogenic acid mitigates ferroptosis in macrophages induced by pneumolysin and streptococcus pneumoniae through activation of NRF2/GPX4 pathway.
Article in BMC immunology, 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.
- Safe dosage and potential risks of chlorogenic acid: insights fromFrontiers in pharmacology · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDrug-resistant Streptococcus pneumoniae (SP) infections pose a significant global health threat, with a limited availability of effective treatments to prevent disease progression. Chlorogenic acid (CGA) exhibits potent antioxidant and antimicrobial properties, though its exact mechanisms in combating bacterial infections remain not yet fully elucidated. Pneumolysin (PLY), a pivotal virulence factor of SP, specifically contributes to the pathogenesis of these infections. PURPOSE: This study aimed to investigate the role of SP-derived PLY in triggering macrophage ferroptosis and to elucidate the potential mechanism underlying CGA-mediated regulation of this process.
methodsA macrophage-SP co-culture model was established to investigate PLY-induced ferroptosis and the mechanisms underlining CGA-mediated antimicrobial effects. Hemolysis assays were conducted to assess PLY activity, and macrophage apoptosis was evaluated using an Annexin V/PI apoptosis detection kit and CCK-8 assay. Key biomarkers, including intracellular ROS levels, mitochondrial membrane potential, MDA content, and total iron levels, were measured using commercial assay kits. Transmission electron microscopy (TEM) was utilized to analyze mitochondrial ultrastructural alterations, particularly morphological changes in the mitochondrial membrane and cristae. Additionally, the expression of key ferroptosis-related factors was analyzed via qRT-PCR, Western blotting, and immunofluorescence staining to delineate the underlying molecular pathways.
resultsCGA markedly suppressed SP proliferation and attenuated PLY activity. Co-culture with SP or PLY exposure significantly decreased macrophage viability and triggered apoptotic cell death, whereas CGA treatment markedly attenuated apoptosis. CGA upregulated the expression of Nrf2, SOD1, and HO-1 while substantially decreasing intracellular ROS accumulation. Additionally, CGA preserved mitochondrial membrane integrity and significantly lowered MDA content and total iron levels in macrophages. Furthermore, CGA significantly upregulated the expression of key ferroptosis-related factors, including GPX4 and SLC7A11.
conclusionsCGA effectively attenuates SP-induced macrophage ferroptosis by activating the Nrf2/GPX4 signaling axis. Notably, PLY was identified as a critical mediator of SP-induced macrophage ferroptosis, and further investigations are warranted to elucidate the exact molecular mechanisms.
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.