Inhibition of inducible nitric oxide synthase and interleukin-1β expression by tunicamycin in cultured glial cells exposed to lipopolysaccharide.

Endoplasmic reticulum (ER) stress has recently been implicated in human diseases such as Alzheimer׳s disease (AD) and Parkinson׳s disease (PD). However, the link between the immune system, ER stress, and the development of neurodegenerative diseases has not yet been clarified in detail. Mouse primary cultured astrocytes were treated with lipopolysaccharide (LPS) and/or tunicamycin (Tm), and inducible nitric oxide synthase (iNOS) and interleukin (IL)-1β levels were then measured using RT-PCR, ELISA, and Western blotting.

ER stress upregulated PGE₂/IFNγ-induced IL-6 expression and down-regulated iNOS expression in glial cells.

The disruption of endoplasmic reticulum (ER) function can lead to neurodegenerative disorders, in which inflammation has also been implicated. We investigated the possible correlation between ER stress and immune function using glial cells. We demonstrated that ER stress synergistically enhanced prostaglandin (PG) E₂ + interferon (IFN) γ-induced interleukin (IL)-6 production.