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Background <p>Platelets and platelet-derived factors are increasingly recognised as modulators of immune and inflammatory processes beyond haemostasis. However, their effects on astrocyte-like glial cells under basal and infection-mimicking conditions remain incompletely characterised in vitro.</p> Methods and results <p>In this study, B92 glial cells were exposed to platelet-rich plasma (PRP; 0–20%) under basal conditions or in the presence of heat-killed <i>Escherichia coli</i> (HKEC) as an infection-mimicking inflammatory stimulus. After 24&#xa0;h of treatment, cellular metabolic activity (MTT), lysosomal/endocytic activity (neutral red uptake), oxidative stress (NBT reduction), and transcriptional expression of selected cytokines (TNF-α, IL-10, IL-1β) and apoptosis-related genes (BAX, Caspase-3, BCL-2) were assessed. PRP induced dose-dependent changes in metabolic activity and oxidative stress markers under both experimental conditions. At the transcriptional level, PRP exposure was associated with reduced TNF-α and increased IL-10 expression, while IL-1β expression showed limited attenuation, particularly under HKEC stimulation, indicating a mixed and context-dependent immunomodulatory profile. PRP treatment was also associated with altered expression of apoptosis-related genes, characterised by increased BCL-2 and reduced BAX and Caspase-3 mRNA levels, without direct functional validation of apoptotic outcomes.</p> Conclusions <p>These findings demonstrate that PRP modulates metabolic activity, oxidative stress, and inflammatory gene expression in B92 glial cells under basal and infection-mimicking conditions in vitro. The results support a context-dependent immunomodulatory effect of PRP-derived factors at the transcriptional and functional assay level. Given the exclusive use of an immortalised glial cell line and the absence of platelet-specific and functional apoptosis controls, the findings should be interpreted as descriptive and hypothesis-generating, warranting further mechanistic and in vivo investigation.</p>

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Immunomodulatory effects of platelet-rich plasma on inflammatory and metabolic responses of B92 glial cells exposed to heat-killed Escherichia coli

  • 期刊论文

  • 发表日期：

    2026年2月7日

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  • Mahtab Pourkamalzadeh,
  • Seyyed Meysam Abtahi Froushani

摘要

Background

Platelets and platelet-derived factors are increasingly recognised as modulators of immune and inflammatory processes beyond haemostasis. However, their effects on astrocyte-like glial cells under basal and infection-mimicking conditions remain incompletely characterised in vitro.

Methods and results

In this study, B92 glial cells were exposed to platelet-rich plasma (PRP; 0–20%) under basal conditions or in the presence of heat-killed Escherichia coli (HKEC) as an infection-mimicking inflammatory stimulus. After 24 h of treatment, cellular metabolic activity (MTT), lysosomal/endocytic activity (neutral red uptake), oxidative stress (NBT reduction), and transcriptional expression of selected cytokines (TNF-α, IL-10, IL-1β) and apoptosis-related genes (BAX, Caspase-3, BCL-2) were assessed. PRP induced dose-dependent changes in metabolic activity and oxidative stress markers under both experimental conditions. At the transcriptional level, PRP exposure was associated with reduced TNF-α and increased IL-10 expression, while IL-1β expression showed limited attenuation, particularly under HKEC stimulation, indicating a mixed and context-dependent immunomodulatory profile. PRP treatment was also associated with altered expression of apoptosis-related genes, characterised by increased BCL-2 and reduced BAX and Caspase-3 mRNA levels, without direct functional validation of apoptotic outcomes.

Conclusions

These findings demonstrate that PRP modulates metabolic activity, oxidative stress, and inflammatory gene expression in B92 glial cells under basal and infection-mimicking conditions in vitro. The results support a context-dependent immunomodulatory effect of PRP-derived factors at the transcriptional and functional assay level. Given the exclusive use of an immortalised glial cell line and the absence of platelet-specific and functional apoptosis controls, the findings should be interpreted as descriptive and hypothesis-generating, warranting further mechanistic and in vivo investigation.