title: The impact of infectious diseases upon neuroendocrine circuits.
abstract: During infectious diseases, neuroendocrine and immune networks act in concert, facilitating host response. It is known that infections cause profound immune changes, but the impact upon immunoendocrine circuits has been less studied. Disorders in the hypothalamic-pituitary-adrenal (HPA) axis were frequently observed associated with infections, and these changes often occur in parallel to alterations in the systemic cytokine network. Explanations for the infection-associated immunoendocrine disturbances include several and not mutually exclusive possibilities. Changes in cytokine levels can enhance or suppress the HPA axis, by acting at the hypothalamus-pituitary unit and/or at the adrenal glands. In situ inflammatory reactions or structural changes like vascular alterations or an enhanced extracellular matrix deposition in the endocrine microenvironment may also lead to a transient HPA dysfunction. Lastly, a microbe-related effect by means of pathogen infiltration or exploitation of the host's hormonal microenvironment may be involved as well. A better understanding of the relevance of immunoendocrine communication during infectious diseases, and how disturbances in the flux of information lead to neuroendocrine immune-related disorders will provide important insights into mechanisms underlying the disease pathology.
authors.affiliation: Institute of Immunology, School of Medical Sciences, National University of Rosario, Rosario, Argentina. perez_anarosa@yahoo.com.ar
authors.forename: Ana Rosa
authors.initials: AR
authors.lastname: Pérez
authors.forename: Oscar
authors.initials: O
authors.lastname: Bottasso
authors.forename: Wilson
authors.initials: W
authors.lastname: Savino
mesh_terms: D000818:Animals; D002417:Cattle; D003141:Communicable Diseases / Q000503:physiopathology*; D016207:Cytokines / Q000502:physiology*; D003687:Dehydroepiandrosterone / Q000502:physiology; D016326:Extracellular Matrix Proteins / Q000502:physiology; D005260:Female; D005938:Glucocorticoids / Q000502:physiology; D006728:Hormones / Q000502:physiology*; D006790:Host-Parasite Interactions / Q000276:immunology / Q000502:physiology; D054884:Host-Pathogen Interactions / Q000502:physiology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology; D008297:Male; D051379:Mice; D018448:Models, Immunological; D010215:Papio; D010273:Parasitic Diseases, Animal / Q000276:immunology / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D013312:Stress, Physiological / Q000276:immunology / Q000502:physiology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D016207:Cytokines; D016326:Extracellular Matrix Proteins; D005938:Glucocorticoids; D006728:Hormones; D003687:Dehydroepiandrosterone