Inflammatory Disease as Chronic Stress
ABSTRACT It is now established that communication between the CNS and the immune system is bidirectional, that endocrine factors can alter immune function and that immune responses can alter both endocrine and CNS responses. In many respects CNS and endocrine responses to acute inflammation are similar to the changes associated with acute stress exposure. In contrast, during chronic inflammation associated with adjuvant induced arthritis (AA), although circulating levels of corticosterone are increased, the peptidergic regulation of the hypothalamus is different from that seen during acute stress. As the disease progresses, a paradoxical reduction occurs in CRH mRNA in the paraventricular nucleus (PVN), whereas PVN AVP mRNA increases. These data suggest that there is increased expression of AVP mRNA within the CRH cells of the PVN with an increased emphasis on AVP regulation of HPA output. Additionally, HPA function is altered during chronic inflammation such that responses to psychological stress (i.e. restraint) are significantly dampened, while responses to further inflammatory challenges are maintained. These data suggest that alterations in PVN peptide colocalization may be important in regulating the progression of peripheral inflammatory responses and that the effects of inflammation on the hypothalamus alter stress-responsive systems. In addition to the AA model, we have similarly observed alterations in PVN peptide mRNA expression with disease onset in the murine MRL lpr/lpr and MRL +/+ model of SLE. Disease onset in murine SLE is spontaneous and does not rely on exogenous application of adjuvant; however, decreased levels of CRH in the PVN were observed from early disease onset in this animal model. It is suggested that alterations in CRH regulation in response to either acute or chronic inflammation may contribute as etiological factors to both psychiatric (i.e. neuropsychiatric SLE) and stress-related disease.
SourceAvailable from: Taisuke Ito[Show abstract] [Hide abstract]
ABSTRACT: Alopecia areata is considered to be a cell-mediated autoimmune disease, in which autoreactive cytotoxic T cells recognize melanocyte-associated proteins such as tyrosinase. This review discusses recent advances in the understanding of the pathogenesis of alopecia areata, focusing on immunobiology and hormonal aspects of hair follicles (HFs). The HF is a unique "miniorgan" with its own immune and hormonal microenvironment. The immunosuppressive milieu of the anagen hair bulb modulated by immunosuppressive factors is known as "hair follicle immune privilege." The collapse of the hair follicle immune privilege leads to autoimmune reactions against hair follicle autoantigens. Alopecia areata is sometimes triggered by viral infections such as influenza that causes excess production of interferons (IFN). IFN- γ is one of the key factors that lead to the collapse of immune privilege. This paper reviews the interactions between the endocrine and immune systems and hair follicles in the pathogenesis of alopecia areata.Clinical and Developmental Immunology 09/2013; 2013:348546. DOI:10.1155/2013/348546 · 2.93 Impact Factor
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ABSTRACT: Una parte preponderante della popolazione adulta soffre o ha sofferto in più occasioni di sintomatologia vaga ed aspecifica (MUS, Medically Unexplained Symptoms, secondo la definizione più accreditata dalla letteratura internazionale), categoria alla quale si riconduce una larga famiglia di disturbi di varia natura, che solo raramente sfocia in una diagnosi precisa, mantenendosi piuttosto di frequente entro i limiti di quadri clinici alterati, ma non al punto da apparire patologici. La letteratura in materia ha conosciuto un notevole sviluppo dagli anni Ottanta ad oggi, prevalentemente a causa della crescente incidenza del fenomeno, considerato al giorno d'oggi come una delle problematiche più frequenti, dispendiose e di più complessa gestione nell'ambito della medicina generale. • alterazione della funzionalità della tiroide, • disturbi ormonali aspecifici; • disturbi funzionali a carico dell'apparato cardio-circolatorio (es. ipertensione, ipotensione); • cambio delle masse corporee non associate a cambiamenti nutrizionali (alterazioni metaboliche); • irritabilità psicofisica; • abbassamento delle difese immunitarie con maggiore vulnerabilità alle malattie; • cefalee; • problemi dermatologici; • disturbi della sfera sessuale. Alcuni disturbi riconducibili all'area dei MUS Uno degli scogli iniziali rispetto alla formulazione di un approccio al fenomeno, è stato probabilmente il confinamento di questo genere di problematiche all'interno di una non meglio precisata area di disturbi psicosociali dai quali il medico generalista si discostava ritenendoli indirizzabili verso discipline specialistiche. I passi in avanti compiuti nell'analisi delle interazioni fra i sistemi nervoso, endocrino ed immunitario, hanno dato vita a nuovi orizzonti nell'ambito della pratica clinica della medicina generale; in particolare grazie all'integrazione della copiosa letteratura in materia di stress.
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ABSTRACT: Chronic noncancer pain (CNCP) is a common and complex disorder associated with declines in physical health and functional status, emotional well-being, and quality of life. To best address the complexity of this condition, research and clinical practice for CNCP should be guided by a framework incorporating both biologic and psychologic factors. This article presents a biobehavioral model of chronic pain that hypothesizes mechanisms related to the effectiveness of a complementary therapy, guided imagery (GI), for this population. Using the research-to-model/theory strategy, we mapped findings from published reports of interdisciplinary research into physiologic and psychologic aspects of the nature and mechanisms of pain, as well as the use of GI for pain, to build the model of GI's effects on pain, pain disability, and depression. In the model, these outcomes of GI for persons experiencing CNCP are mediated by psychologic (pain self-efficacy and pain beliefs) and physiologic (immune-mediated analgesia and sickness response) variables. A biobehavioral approach to nursing phenomena will advance understanding of health and health-related issues and has the potential to improve outcomes through delineation of mechanisms underlying relationships between psychologic and biologic factors. Increased consumer use of complementary therapies to treat pain, the current cost-driven health care system, and the mandate for evidence-based practice support the need to validate the efficacy of such therapies. This empirically derived model provides a framework for practice and research for nurses and other health care providers to promote health, function, and well-being in persons with CNCP.Pain management nursing: official journal of the American Society of Pain Management Nurses 12/2013; 14(4):368-78. DOI:10.1016/j.pmn.2011.08.001 · 1.79 Impact Factor