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Introduction: Mast cells (MCs) are tissue-resident immune cells implicated in antibacterial responses. These include chemokine secretion, degranulation, and the release of mast cell-extracellular traps, which are primarily dependent on reactive oxygen species (ROS) production. Our study investigated whether human mast cells (hMCs) develop individual response patterns to bacteria located at different tissue sites: Escherichia coli (gut commensal), Listeria monocytogenes (foodborne intracellular pathogen), Staphylococcus aureus (skin commensal and opportunistic pathogen), and Streptococcus pneumoniae (upper respiratory tract commensal and lung pathogen).
Methods: After live bacteria exposure, hMCs were analyzed by a combined flow cytometry assay for degranulation, ROS production, DNA externalization, and for β-hexosaminidase, chemokine, and prostaglandin release.
Results: L. monocytogenes induced hMC degranulation, IL-8 and MCP-1 release coupled with DNA externalization in a novel hMC ROS independent manner. In contrast, S. pneumoniae caused ROS production without DNA release and degranulation. E. coli induced low levels of hMC degranulation combined with interleukin 8 and MCP-1 secretion and in the absence of ROS and DNA externalization. Finally, S. aureus induced hMCs prostaglandin D2 release and DNA release selectively. Our findings demonstrate a novel hMC phenomenon of DNA externalization independent of ROS production. We also showed that ROS production, degranulation, DNA externalization, and mediator secretion occur as independent immune reactions in hMCs upon bacterial encounter and that hMCs contribute to bacterial clearance.
Conclusions: Thus, hMCs exhibit a highly individualized pattern of immune response possibly to meet tissue requirements and regulate bacteria coexistence vs defense.
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http://dx.doi.org/10.1002/iid3.295 | DOI Listing |
BMB Rep
September 2025
Basic Research Laboratory, Department of Physiology, College of Medicine, Smart Marine Therapeutic Center, Cardiovascular and Metabolic Disease Core Research Center, Inje University, Busan 47392, Korea; Department of Health Science and Technology, College of Medicine, Inje University, Busan 47392, K
Patients with multiple myeloma develop resistance to thalidomide during therapy, and the mechanisms to counteract thalidomide resistance remain elusive. Here, we explored the interaction between cereblon and mitochondrial function to mitigate thalidomide resistance in multiple myeloma. Measurements of cell viability, ATP production, mitochondrial membrane potential, mitochondrial ROS, and protein expression via western blotting were conducted in vitro using KSM20 and KMS26 cells to assess the impact of thalidomide on multiple myeloma.
View Article and Find Full Text PDFToxicol Mech Methods
September 2025
Lung Diseases Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.
Mechanistic studies have been suggested that toxic effects of bleomycin are generally attributed to formation of free radicals, mitochondria damages, oxidative stress and inflammation. For this purpose, we explored the direct exposure of bleomycin and protective effects of the betanin and vanillic acid separately against its possible toxicity in rat lung isolated mitochondria. Various mitochondrial toxicity parameters were evaluated including; succinate dehydrogenases (SDH) activity, reactive oxygen species (ROS) formation, mitochondrial swelling, mitochondrial membrane potential (MMP) collapse, malondialdehyde (MDA) and glutathione disulfide (GSSG) levels.
View Article and Find Full Text PDFCNS Neurosci Ther
September 2025
Affiliated Rehabilitation Hospital, Jiang Xi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Objective: Traumatic brain injury (TBI), a prevalent neurological disorder worldwide, is marked by varying degrees of neurological dysfunction. A key contributor to secondary damage and impediments in the repair process is the unregulated activation of microglia, which triggers neuroinflammation. Emerging evidence highlights the therapeutic potential of transcranial pulsed current stimulation (tPCS) in mitigating neurological deficits.
View Article and Find Full Text PDFImmunopharmacol Immunotoxicol
September 2025
Neuroscience Research Center, Suleyman Demirel University, Isparta, Türkiye.
Background: Microglia are brain resident cells that control neural network maintenance, damage healing, and brain development. Microglia undergo apoptosis, cytokine production, and reactive free radicals of oxygen (ROS) in response to lipopolysaccharide (LPS) stimulation. TRPM2 is activated by LPS-induced oxidative stress, but it is inhibited by carvacrol (CARV) and N-(p-amylcinnamoyl)anthranilic acid (ACA).
View Article and Find Full Text PDFBiochem Biophys Res Commun
September 2025
Departamento de Ciencias Químico-Biológicas, Instituto de Ciencias Biomédicas, Universidad Autónoma de Ciudad Juárez, Ciudad Juárez, Mexico. Electronic address:
Chlorpromazine (CPZ) is a first-generation antipsychotic that has been widely used to treat an array of neurological conditions, including schizophrenia, bipolar disorder, and anxiety. Treatment of these chronic conditions with CPZ has been linked to elevated levels of reactive oxygen species (ROS), and accumulating evidence supports a link between ROS and chronic and degenerative pathologies, including cardiovascular diseases. Therefore, the aim of this study was to observe the presence of oxidative stress in porcine aortic endothelial cells (PAE) exposed to different concentrations of CPZ in vitro.
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