The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system.
- I. Elenkov, R. Wilder, G. Chrousos, E. Vizi
- BiologyPharmacological Reviews
- 1 December 2000
The activation of SNS during an immune response might be aimed to localize the inflammatory response, through induction of neutrophil accumulation and stimulation of more specific humoral immune responses, although systemically it may suppress Th1 responses, and, thus protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages.
The Pathophysiologic Roles of Interleukin-6 in Human Disease
- D. Papanicolaou, R. Wilder, S. Manolagas, G. Chrousos
- Medicine, BiologyAnnals of Internal Medicine
- 15 January 1998
What makes interleukin-6 particularly interesting to physicians is its marked pleiotropy and its involvement not only in inflammation but in the regulation of endocrine and metabolic functions.
Histamine potently suppresses human IL-12 and stimulates IL-10 production via H2 receptors.
- I. Elenkov, E. Webster, D. Papanicolaou, T. Fleisher, G. Chrousos, R. Wilder
- Biology, MedicineJournal of Immunology
- 1 September 1998
It is reported that histamine dose-dependently inhibited the secretion of human IL-12 and increased the production of IL-10 in LPS-stimulated whole blood cultures and may represent a novel mechanism by which excessive secretion of histamine potentiates Th2-mediated allergic reactions and contributes to the development of certain infections and tumors normally eliminated by Th1-dependent immune mechanisms.
Expression of cyclooxygenase-1 and -2 in human colorectal cancer.
- H. Sano, Y. Kawahito, T. Hla
- Biology, MedicineCancer Research
- 1 September 1995
The data suggest that the enhanced expression of the COX-2 gene in Colon cancer tissues may contribute to the enhanced synthesis of prostaglandin E2 by the colon cancer tissues.
Inflammatory mediator-induced hypothalamic-pituitary-adrenal axis activation is defective in streptococcal cell wall arthritis-susceptible Lewis rats.
- E. Sternberg, J. Hill, R. Wilder
- Biology, MedicineProceedings of the National Academy of Sciences…
- 1 April 1989
Findings support the concept that susceptibility of LEW/N rats to SCW arthritis is related to defective HPA axis responsiveness to inflammatory and other stress mediators and that resistance of F344/N Rats to SCw arthritis is regulated by an intact HPAaxis-immune system feedback loop.
Cyclooxygenase-1 and -2 expression in rheumatoid synovial tissues. Effects of interleukin-1 beta, phorbol ester, and corticosteroids.
- L. Crofford, R. Wilder, T. Hla
- Biology, MedicineJournal of Clinical Investigation
- 1 March 1994
Modulation of Cox-2 expression by IL-1 beta and corticosteroids may be an important component of the inflammatory process in synovial tissues from patients with RA.
Induction of vascular endothelial growth factor expression in synovial fibroblasts by prostaglandin E and interleukin‐1: a potential mechanism for inflammatory angiogenesis
- P. Ben-Av, L. Crofford, R. Wilder, T. Hla
- Biology, MedicineFEBS Letters
- 18 September 1995
Hypothalamic-pituitary-adrenal axis perturbations in patients with fibromyalgia.
- L. Crofford, S. Pillemer, R. Wilder
- Medicine, BiologyArthritis & Rheumatism
- 1 November 1994
The view that HPA axis function is perturbed in patients with FM is supported, with a significant decrease in net integrated cortisol response to oCRH in FM patients, indicating adrenal hyporesponsiveness.
Corticotropin releasing hormone related behavioral and neuroendocrine responses to stress in Lewis and Fischer rats
- E. Sternberg, J. Glowa, P. Gold
- Biology, PsychologyBrain Research
- 20 January 1992
Modulatory effects of glucocorticoids and catecholamines on human interleukin-12 and interleukin-10 production: clinical implications.
- I. Elenkov, D. Papanicolaou, R. Wilder, G. Chrousos
- Biology, MedicineProceedings of the Association of American…
- 1 September 1996
It is suggested that the central nervous system may regulate IL-12 and IL-10 secretion and, hence, TH1/TH2 balance via the peripheral end-effectors of the stress system, which may cause a selective suppression of TH1 functions and a shift toward a TH2 cytokine pattern rather than generalized TH suppression.
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