Expression of toll-like receptors and inflammatory mediators in primary human glioma cells (low- and high-grade) compared to primary cells from epileptic human brain.

Toll-like receptors (TLRs) have been implicated in the pathogenesis of glioma as principal regulators of inflammation and innate immune function. Considering the heterogeneous nature of gliomas, ranging from low to high grade with different therapeutic responses, investigating the differences in the levels of TLR2 and TLR4 and associated inflammatory markers in these distinct groups is of great clinical significance. In this study, we investigated changes in the protein expression levels of TLR2 and TLR4, along with key inflammatory mediators, including nuclear factor kappa B (NF-κB) as a downstream signaling molecule, and tumor necrosis factor-alpha (TNF-α), a target of NF-κB activation, by using western blotting. Primary human cells were isolated from surgically resected tissue samples of patients with low- and high-grade gliomas and were compared to cells derived from the human epileptic brain. In vitro cell characterization was performed via immunocytochemistry using markers specific to each group. Protein levels were assessed by western blotting. TLR2 expression was significantly higher in the high-grade glioma group compared to the low-grade group. The expression of TLR2 and TLR4 was significantly greater in the epilepsy group compared to the low-grade glioma group. No remarkable differences were detected in the levels of NF-κB and TNF-α between high and low-grade gliomas. Our results revealed distinct patterns of TLR expression between low- and high-grade gliomas, underscoring the potential involvement of TLRs in the cellular heterogeneity of gliomas.