Posttraumatic stress disorder (PTSD) is a complex and heterogenous condition caused by a noxious psychological trauma and can persist for lengthy periods. Biological sequelae for PTSD include stress-related neuroinflammatory reactions such as activation of glial cells and their subtypes (e.g., astrocytes, microglia, oligodendrocytes, monocytes, and others). Glial cells make up around half the mass of our brains so their potential involvement in PTSD is important. However, emerging evidence including studies of biomarkers for neuroglial activation such as glial fibrillary acidic protein (GFAP) suggest that persistent stress from chronic PTSD can raise the threshold for neuroglial activation, rendering a neuroimmune environment that is significantly more quiescent than normal. This challenging new perception for neuroimmune suppression in chronic individuals with PTSD highlights the beneficial roles that neuroinflammatory responses can have when responding to noxious insults by engaging reparatory neuroglial mechanisms that normally respond to physical and/or mental injury.