Unveiling Anxiety and Post-Traumatic Stress Disorder in Healthcare Workers Through Pre-Employment Evaluations.

Astrocytes are glial cells that play essential roles in the normal functioning of the central nervous system (CNS). Their diverse functions in maintaining brain homeostasis include regulating blood flow, providing metabolic and antioxidant support to neurons, secreting pro- and anti-inflammatory molecules, regulating ionic and neurotransmitter balance, and controlling immune cell activation (; ; ; ). In addition, as immunocompetent cells, astrocytes can express damage-associated molecular patterns (DAMP) and pathogen-associated molecular pattern (PAMP) receptors by undergoing “reactive transformation” (). Reactive astrogliosis represents a defensive process in which astrocytes undergo a series of changes to minimize and repair damage. During such reactive states, astrocytes experience morphological, molecular, cellular, and functional changes, reflecting the heterogeneity of their responses to various factors. For example, reactive astrocytes can exert neuroprotective effects by promoting blood–brain barrier (BBB) repair, sequestering infections via glial scarring, and facilitating metabolic support for surviving neurons () However, this reactivity can also generate detrimental effects if an imbalance occurs between their neuroprotective and neurotoxic effects, which is often related to the intensity and duration of the inflammatory response (; ; ). Neuroinflammatory responses are driven primarily by a variety of mediators, including cytokines (e.g., IL-1β, IL-6, and TNF-α), second messengers, and reactive oxygen species. Although multiple cell types contribute to the production of these mediators, including microglia, peripheral macrophages, and neurons, astrocytes stand out for their ability to functionally integrate into these processes. Specifically, their strategic localization, functional plasticity, and capacity to amplify inflammatory signals enable them to actively participate in the initiation, modulation, and resolution of neuroinflammation, positioning them as central regulators of the neuroimmune environment (). In addition to signaling, these mediators are essential for neuronal metabolism, immune survival signaling, leukocyte trafficking and other neuroinflammatory processes. Consequently, their dysregulation is a critical factor in the progression of neuroinflammation, neurodegeneration, and demyelination within the CNS (; ). For example, during chronic or pathological neuroinflammation induced by infection, injury, or insult, the integrity of the BBB is compromised by immune cell infiltration, edema, cell death, and increased permeability. As neuroinflammation is associated with severe pathological conditions and may trigger autoimmune responses or neurodegenerative disorders, there is a crucial need to investigate the reactivity and molecular mechanisms underlying the response of astrocytes to different stimuli (; ; )