Inflammatory transcription factors as activation markers and functional readouts in immune-to-brain communication.

摘要: Immune-to-brain communication pathways involve humoral mediators, including cytokines, central modulation by neuronal afferents and immune cell trafficking to the brain. During systemic inflammation these contribute mediating brain-controlled sickness symptoms fever. Experimentally, activation of signaling can be mimicked studied when injecting animals with pathogen associated molecular patterns (PAMPS). One component brain inflammatory response, which leads, for example, fever induction, is transcriptional cells via cytokines PAMPS. We others have spatiotemporal physiological significance transcription factors induction within manifestation Evidence has revealed a role nuclear factor (NF)κB in initiation, signal transducer activator (STAT)3 maintenance NF-interleukin (IL)6 or even termination brain-inflammation Moreover, psychological stressors, such as exposure novel environment, leads increased body core temperature genomic NF-IL6-activation, suggesting potential use NF-IL6-immunohistochemistry multimodal marker NF-IL6 differential activity. In addition, nutritional status, reflected circulating levels cytokine-like hormone leptin, influence immune-to-brain age-dependent changes LPS-induced Overall, remain therapeutically important targets treatment during infectious/non-infectious stress. However, exact requires further investigated.