Abstract

Preliminary studies from our laboratory have shown that we can achieve an enhancement of the NK activity using a classical conditioning paradigm. We believe that conditioned enhancement of IFN levels and NK activity and will try to establish the optimal conditions for the conditioned enhancement. The variables which we would like to consider to optimize the elevations are: 1) The schedule of unconditioned stimulus (US)/conditioned stimulus (CS) association trials, 2) The length of exposure to CS, 3) The number of association trials, 4) The time between association trial and test and 5) Dose of poly I:C (suboptimal doses). We will also attempt to determine the extinction of this response with repeated exposure to CS. These studies are important because they explore the connection between mind and body, and resistance to disease. It has become increasingly apparent that many diseases are multifactorial and psychosocial aspects may play an important role in the etiology of disease. We would like to see this connection between the CNS and resistance to disease exploited for the benefit of the health of the individual, instead of always being a liability (in terms of suppressed immunocompetence when challenged by adverse circumstances). We feel that a conditioned enhancement of immunocompetence may be a possibility for deriving benefit from this connection between mind and immunity.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA037570-07
Application #
2089392
Study Section
Neurology C Study Section (NEUC)
Project Start
1986-02-01
Project End
1995-01-31
Budget Start
1993-02-01
Budget End
1995-01-31
Support Year
7
Fiscal Year
1993
Total Cost
Indirect Cost

  Institution

Name
University of Alabama Birmingham
Department
Microbiology/Immun/Virology
Type
Schools of Dentistry
DUNS #
004514360
City
Birmingham
State
AL
Country
United States
Zip Code
35294

  Publications

Demissie, S; Rogers, C F; Hiramoto, N S et al. (1996) Lipopolysaccharide and IL-1 alpha activate CNS pathways as measured by NK cell activity. Physiol Behav 59:499-504
Ghanta, V K; Hiramoto, N S; Soong, S J et al. (1995) Conditioning of the secondary cytotoxic T-lymphocyte response to YC8 tumor. Pharmacol Biochem Behav 50:399-403
Demissie, S; Rogers, C F; Hiramoto, N S et al. (1995) Arecoline a muscarinic cholinergic agent conditions central pathways that modulate natural killer cell activity. J Neuroimmunol 59:57-63
Hiramoto, R N; Ghanta, V K; Soong, S J et al. (1994) Use of an allogeneic antigen to induce resistance and regression of an autologous tumor. J Immunother Emphasis Tumor Immunol 15:202-11
Kerr, M; Fischer, J E; Purushotham, K R et al. (1994) Characterization of the synthesis and expression of the GTA-kinase from transformed and normal rodent cells. Biochim Biophys Acta 1218:375-87
Hsueh, C M; Tyring, S K; Hiramoto, R N et al. (1994) Efferent signal(s) responsible for the conditioned augmentation of natural killer cell activity. Neuroimmunomodulation 1:74-81
Ghanta, V K; Rogers, C F; Hsueh, C M et al. (1994) Role of arcuate nucleus of the hypothalamus in the acquisition of association memory between the CS and US. J Neuroimmunol 50:109-14
Hsueh, C M; Rogers, C; Hiramoto, R N et al. (1994) Effect of dexamethasone on conditioned enhancement of natural killer cell activity. Neuroimmunomodulation 1:370-6
Rogers, C; Ghanta, V; Demissie, S et al. (1994) Sodium carbonate prevents NK cell conditioning by interfering with the US signal. Int J Neurosci 77:277-86
Rogers, C F; Ghanta, V K; Demissie, S et al. (1994) Lidocaine interrupts the conditioned natural killer cell response by interfering with the conditioned stimulus. Neuroimmunomodulation 1:278-83

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