A research team led by the National Center for Obstetrics and Gynecology at the University of Hokkaido has investigated the role of microorganisms in endotoxic death factors. They found that a peptide called Reg3γ acts as a neurotransmitter that targets the brain that protects the host from endotoxic death.
Sepsis is a highly contagious disease that develops when the body’s immune system causes severe damage. Although the infection caused.inflammatory cytokines Inevitably to eliminate bacteria, dysregulated production of these substances can lead to endotoxic shock. Despite widespread use of anti-TNF-anti antibody administration or glucocorticoids in patients tolerating endotoxic shock, mortality rate was great at 30%. These disastrous results suggest that the endotoxic death process is only explained by mild inflammation.
Study heat neurons normally focus on ion channels. Natural painkillers such as artificial receptor antagonist V 1 channel 1 (TRPV1), and TRP ankyrin 1 (TRPA1) have been described in microbial pathogens and cause pain for protect the organism from harm. Recent reports suggest that low-grade pathogens and TRP channels regulate dermal immune system, psoriasis, ischemic stroke, candidiasis, and osteomyelitis. In engineering, these phenomena are thought to be triggered by paracrine secretion of nociceptor-derived peptides such as Calcitonin peptide-binding protein (CGRP) and VIP, which regulate immune signals and endocrine pathways. These findings also raise the question of whether there are “hormones” derived from neurons.
In this new study, Dr. Kenta Maruyama at NIPS, Assistant Professor Takeshi Kondo at the University of Hokkaido, and colleagues stated that Reg3γ peptide derived from neurons enters the inflammatory brain and inhibits the expression of microglial IDO1, a key enzyme of the kynurenine pathway. Endotoxin-induced neuron-null mice and Reg3γ-deficient mice with neuron-specific mice exhibit higher mortality with decreased HK1 brain phosphorylation and ATP production despite normal inflammation. This metabolism is observed only in the brain, and an increase in the brain’s quinolinic acid, a neurotoxic metabolite of the kynurenine pathway, results in the killing of HK1. In particular, Reg3γ brain control protects mice from endotoxic death by proliferation brain ATP production. By identifying Reg3γ-derived neurons as the target hormone for microglia, this study sheds new light on patient perception of endotoxic death.
The study was published in Cell Report.
Kenta Marumama, Nociceptor-derived Reg3g prevents endotoxic death by targeting kynurenine pathway in microglia, Cell Report (2022). DOI: 10.1016 / j.celrep.2022.110462
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Pain neuron-derived peptide prevents endotoxic death by targeting kynurenine pathway in microglia Source link Pain neuron-derived peptide prevents endotoxic death by targeting kynurenine pathway in microglia