The astroglial-derived S100β protein stimulates the expression of nitric oxide synthase in rodent macrophages through p38 MAP kinase activation

Palmitoylethanolamide improves colon inflammation through an enteric glia/toll like receptor 4-dependent PPAR-α activation

“…This is confirmed by the observation that PEA is able to counteract the expression and release of proinflammatory markers from EGCs stimulated with exogenous S100B. Since enteroglial S100B can also increase macrophage activity causing a massive proinflammatory response during colitis,40 specific inhibition of S100B release may be a key event in the effort to block gut inflammation.…”

REMOVAL: Elevated serum S100B protein in first-episode drug-naïve Chinese patients with schizophrenia

“…Additionally, Sarandol et al (2007) found that serum S100B levels were significantly correlated with RBC-SOD activities and plasma MDA in the patient group. The importance of S100B in the induction of oxidative stress is supported in the literature (Esposito et al, 2006). Future studies should address the relationships between S100B, BDNF, and oxidative stress in schizophrenia.…”

Glial alterations in tuberculous and cryptococcal meningitis and their relation to HIV co-infection – A study on human brains

“…Several earlier studies have established that S-100β exerts a neuroprotective and neurotrophic influence at nanomolar concentrations [25][26][27], but at micromolar concentrations it is toxic, leading to astrocytic and neuronal death [22,28]. Esposito et al [29] observed that S-100β protein initiates a gliotic response by inducing the release of pro-inflammatory mediators such as nitric oxide (NO) and cytokines from the microglia and astrocytes, which sequentially are deleterious to neurons. It is likely that S-100β-labeled reactive astrocytes and the diffuse neuropil labeling noted in the cortical grey matter and hippocampus in cases of TBM and CM may have a slowly evolving toxic effect with apoptosis on neurons, though not overtly evident.…”