Infectious immunity in the central nervous system and brain function

Abstract

Inflammation is emerging as a critical mechanism underlying neurological disorders of various etiologies, yet its role in altering brain function as a consequence of neuroinfectious disease remains unclear. Although acute alterations in mental status due to inflammation are a hallmark of central nervous system (CNS) infections with neurotropic pathogens, post-infectious neurologic dysfunction has traditionally been attributed to irreversible damage caused by the pathogens themselves. More recently, studies indicate that pathogen eradication within the CNS may require immune responses that interfere with neural cell function and communication without affecting their survival. In this Review we explore inflammatory processes underlying neurological impairments caused by CNS infection and discuss their potential links to established mechanisms of psychiatric and neurodegenerative diseases.

Astrocyte-derived lipoxins A4 and B4 promote neuroprotection from acute and chronic injury

“…Neurodegeneration in response to stress or injury has been associated with both the induction of neuroinflammatory signals (34)(35)(36)(37) and a corresponding loss of homeostatic prosurvival cues (38)(39)(40)(41). However, the mechanisms by which these activities are coordinated in the CNS remain unclear.…”

Engineering challenges for brain tumor immunotherapy

“…Cerebrospinal fluid (CSF), produced by choroid plexus cells in the ventricles, bathes the brain parenchyma and flows in the subarachnoid space (the space between the pia mater and arachnoid mater). Immunity in the CNS is very tightly regulated, and during homeostasis, T-cells and other myeloid cells that reside in the meningeal layers, exert their immunogenic effects from there [13,14]. One way to understand neuroimmunology is to embrace the concept that the purpose of the immune reaction in CNS pathology is to allow neurons to function undisturbed.…”

“…During homeostasis, blood-borne immune cells do not cross the BBB [13,14,18]. In pathological states, however, the primary entry site of immune cells is via the meningeal blood vessels, across the BMB, into the pia to infiltrate the brain parenchyma using a variety of mechanisms, not all of which are fully understood [13].…”

“…In pathological states, however, the primary entry site of immune cells is via the meningeal blood vessels, across the BMB, into the pia to infiltrate the brain parenchyma using a variety of mechanisms, not all of which are fully understood [13]. During infection, pathogens may initially gain access to the CSF across vessels within the meninges and ventricular system, due to the fenestrated endothelium [13,14]. However, the meningeal arachnoid membrane and ventricular choroid plexus epithelial cells have intercellular tight junctions that help restrict the invasion of pathogens into the CNS parenchyma [15–17].…”

Not all scientists are raised equal

“…0161). Indeed, even within scientific functions such as conferences, women scientists systematically get the short end of the stick both in terms of active contributions 13 (https://cswa.aas.org/percent.html) and in how the 'air is shared' in discussion and question and answer sessions (see the Comment by Sarah Schmidt and James Davenport; article no. 0153).…”