Stress-linked psychiatric disorders, including anxiety and major depressive disorder, are associated with systemic inflammation. Recent studies have reported stress-induced alterations in haematopoiesis that result in monocytosis, neutrophilia, lymphocytopenia and, consequently, in the upregulation of pro-inflammatory processes in immunologically relevant peripheral tissues. There is now evidence that this peripheral inflammation contributes to the development of psychiatric symptoms as well as to common co-morbidities of psychiatric disorders such as metabolic syndrome and immunosuppression. Here, we review the specific brain and spinal regions, and the neuronal populations within them, that respond to stress and transmit signals to peripheral tissues via the autonomic nervous system or neuroendocrine pathways to influence immunological function. We comprehensively summarize studies that have employed retrograde tracing to define neurocircuits linking the brain to the bone marrow, spleen, gut, adipose tissue and liver. Moreover, we highlight studies that have used chemogenetic or optogenetic manipulation or intracerebroventricular administration of peptide hormones to control somatic immune responses. Collectively, this growing body of literature illustrates potential mechanisms through which stress signals are conveyed from the CNS to immune cells to regulate stress-relevant behaviours and comorbid pathophysiology.

Malignant tumors constitute a major global public health burden. Chronic psychological stress (CPS) manifests as sustained dysregulation arising from prolonged adaptive responses to chronic endogenous and exogenous stimuli. Clinical evidence indicates that CPS markedly influences cancer progression, with most oncology patients developing detectable stress-related psychological disorders during disease management. This review synthesizes recent advances in understanding CPS-mediated oncogenic mechanisms and evaluates current intervention approaches. Mechanistically, CPS compromises immune surveillance through neuroendocrine-mediated hormonal dysregulation, impairing malignant cell recognition and clearance. Concurrently, CPS hormones promote tumor metabolic adaptation via hypothalamic-pituitary-adrenal axis-driven metabolic reprogramming, enhancing glycolytic flux to support uncontrolled proliferation. CPS further accelerates tumor progression through reactive oxygen species-induced mitochondrial impairment, DNA damage accumulation, and inflammatory cascades. Notably, CPS induces gut microbiota perturbations that reciprocally amplify tumorigenic processes through microbial metabolite disturbances and neuroimmune crosstalk, creating a self-perpetuating pathogenic loop. Therapeutic strategies to address cancer-related CPS that encompass pharmacological agents targeting neuroendocrine pathways, psychosomatic behavioral interventions, social environment adjustments, and evidence-based traditional Chinese medicine formulations demonstrate potential in cancer prevention, treatment, and outcome optimization. However, challenges remain in achieving precise neuromodulation and minimizing intervention side effects, underscoring the need for mechanism-guided therapeutic innovations.

Chronic stress, a sustained psychophysiological state, promotes tumor progression primarily by disrupting anti-tumor immunity. Through persistent activation of the HPA axis and sympathetic nervous system, stress hormones such as glucocorticoids and catecholamines reshape the tumor microenvironment and systemically impair immune surveillance. This leads to suppressed activity of cytotoxic lymphocytes, expansion of immunosuppressive cells, and ultimately, enhanced immune evasion and metastasis. Furthermore, these pathways undermine the efficacy of conventional and emerging therapies by fostering multidrug resistance. This review highlights these mechanisms and discusses the promise of targeting stress signaling, through both pharmacological and behavioral interventions, as a strategy to improve cancer outcomes. To address the current lack of clinical guidelines for counteracting the cancer progression mediated by chronic stress, this review propose a tiered screening and intervention model based on easily accessible biostress biomarkers. This hypothesis aims to bridge the gap between basic mechanism research and clinical application, providing a theoretical foundation directional guidance for future research.

circumstances. When stressed by stimuli that alter an organism's environment, multiple systems respond across the body. In humans and most mammals, the autonomic Stress, whether physiological, biological or psychological, is an organism's response to a stressor, such as an environmental condition or change in life circumstances. When stressed by stimuli that alter an organism's environment, multiple systems respond across the body. In humans and most mammals, the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis are the two major syste Stress, whether physiological, biological or psychological, is an organism's response to a stressor, such as an environmental condition or change in life circumstances. When stressed by stimuli that alter an organism's environment, multiple systems respond across the body. In humans and most mammals, the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis are the two major systems that respond to stress. Two well-known hormones that humans produce during stressful situations are adrenaline and cortisol. The sympathoadrenal medullary axis (SAM) may activate the fight-or-flight response through the sympathetic nervous system, which dedicates energy to more relevant bodily systems to acute adaptation to stress, while the parasympathetic nervous system returns the body to homeostasis. The second major physiological stress-response center, the HPA axis, regulates the release of cortisol, which influences many bodily functions, such as metabolic, psychological and immunological functions. The SAM and HPA axes are regulated by several brain regions, including the limbic system, prefrontal cortex, amygdala, hypothalamus, and stria terminalis. Through these mechanisms, stress can alter memory functions, reward, immune function, metabolism, and susceptibility to diseases. Disease risk is particularly pertinent to mental illnesses, whereby chronic or severe stress remains a common risk factor for… The…

This type of stress can cause a long-lasting problem called post-traumatic stress disorder (PTSD). How can long term-stress harm my health? People respond to stress in different ways. If you're stressed for a long time you may notice that you are: Getting sick more often than usual because stress weakens your body's ability to fight germs Having stomach problems or trouble digesting food Having trouble sleeping Having headaches Feeling sad, angry, or easily upset When stress keeps going, your body acts as if you're always in danger. That's a lot of strain that may play a part in developing serious health problems, including: Depression Anxiety Heart disease High blood pressure Diabetes It's possible to get used to the symptoms of stress and not even realize there's a problem. So when there's a lot of stress in your life, it's important to pay attention to how it affects you so you can do something about it. How can I manage long-term stress? Simple things that improve your mental health may be helpful in managing long-term stress, such as: Get regular exercise. A 30-minute daily walk can help you feel better and help keep your immune system strong, so you don't get sick.

neurotransmitters and the nerves. IMMUNE SYSTEM The immune system consists of white blood cells patrolling … effect does stress have on our immune system? STRESS AND IMMUNE SYSTEM Stress hormones have the ability … illnesses these studies cover where stress weakens the immune system: colds and respiratory infections