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Pavlovian conditioning of immune function: animal investigation and the challenge of human application

Identifieur interne : 001372 ( Istex/Corpus ); précédent : 001371; suivant : 001373

Pavlovian conditioning of immune function: animal investigation and the challenge of human application

Auteurs : Michael S. Exton ; Anne Kristin Von Auer ; Angelika Buske-Kirschbaum ; Ursula Stockhorst ; Ulrich Göbel ; Manfred Schedlowski

Source :

RBID : ISTEX:1461CF819CB8832BA9C0AB1104B0F9386F240C89

English descriptors

Abstract

Pavlovian conditioning of immune functions provided early impetus to the rapidly expanding knowledge of bi-directional communication among the immune, endocrine, and central nervous systems. Since these early investigations, the phenomenology of this response has been well characterized. However the neural mechanisms and biological relevance of conditioned immunomodulation remain unclear. To this end, we present here data from our laboratories that have: (1) revealed some of the neural mechanisms and biological relevance of an animal model of conditioned immunomodulation; (2) demonstrated the conditionability and potential mechanisms of conditioned immune responses in healthy humans, and (3) investigated conditioned immunomodulation in a clinical sample. Together, these data demonstrate that animal models provide a basis for investigating mechanisms whereby conditioned changes in immune function may modulate health status in a clinical realm.

Url:
DOI: 10.1016/S0166-4328(99)00191-6

Links to Exploration step

ISTEX:1461CF819CB8832BA9C0AB1104B0F9386F240C89

Le document en format XML

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<note type="content">Fig. 1: Conditioned immunomodulation in the rat: conditioning paradigm and experimental groups. Animals received three CS-UCS pairings, followed by three CS reexposures. Animals were sacrificed one hour following the third CS reexposure, with blood and organs removed for immunological analysis.</note>
<note type="content">Fig. 2: Conditioning produces a reduction in splenocyte proliferation (A) and IL-2 production (B) which approaches that effected by cyclosporin administration. Surgical denervation of the spleen blocks the reduced proliferation and cytokine production in conditioned animals, but not in cyclosporin treated rats (C and D). **P<0.01, ***P<0.001.</note>
<note type="content">Fig. 3: (A) Conditioning prolongs the survival time of heart allografts in the rat to a similar magnitude as that achieved by short-course CsA treatment. (B) The addition of sub-therapeutic CsA regime to each group further improves graft survival in conditioned animals only. Importantly, the combination of conditioning and sub-therapeutic CsA therapy produced long-term survival (>100 days) in 20% of animals. Furthermore, the conditioned prolongation of graft survival was completely blocked by prior surgical denervation of the spleen.</note>
<note type="content">Fig. 4: Modulation of NK cell activity (NKCA, in % lysis; effector:target ratio=50:1) in the conditioned group (CS+), UCS control group (UCS), unpaired control group (NC) and saline control group (Sal) five min before and 20 min following CS reexposure (*P<0.05).</note>
<note type="content">Fig. 5: Modulation of the percentage of NK cells following presentation of the CS+ and CS− on acquisition day 3 and 8 (A) and on test days 11, 12 and 13 (B). *P<0.05; **P<0.01.</note>
<note type="content">Fig. 6: Study paradigm. Cycle A and Cycle B represent two consecutive chemotherapeutic cycles. ANV was measured on 2 days (day −2, day −1) prior to the start of a chemotherapeutic cycle. The chemotherapy cycle commenced on day 0. PNV was monitored over 2 days (day +1, day +2) following completion of the cycle. Blood was drawn in cycle B at day −2 (home environment) and at day 0 (hospital) prior to infusion onset. CS, conditioned stimulus; UCS, unconditioned stimulus.</note>
<note type="content">Table 1: Experimental protocol for the conditioning of NK cell activity in healthy humansa</note>
<note type="content">Table 2: Inclusion criteria for conditioning in pediatric cancer patients</note>
<note type="content">Table 3: NK cell activity (NKCA) and plasma cytokine (IFN-γ, IL-1β) concentrations in ANV+ and ANV− patients, measured in the home and in hospital</note>
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<affiliation>Clinic of Pediatric Hematology and Oncology, Heinrich-Heine-University Düsseldorf, PO Box 101007, 40001, Düsseldorf, Germany</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Manfred</namePart>
<namePart type="family">Schedlowski</namePart>
<affiliation>Institute for Medical Psychology, University of Essen, Hufelandstraße 55, 45122, Essen, Germany</affiliation>
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<publisher>ELSEVIER</publisher>
<dateIssued encoding="w3cdtf">2000</dateIssued>
<copyrightDate encoding="w3cdtf">2000</copyrightDate>
</originInfo>
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<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
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<abstract lang="en">Pavlovian conditioning of immune functions provided early impetus to the rapidly expanding knowledge of bi-directional communication among the immune, endocrine, and central nervous systems. Since these early investigations, the phenomenology of this response has been well characterized. However the neural mechanisms and biological relevance of conditioned immunomodulation remain unclear. To this end, we present here data from our laboratories that have: (1) revealed some of the neural mechanisms and biological relevance of an animal model of conditioned immunomodulation; (2) demonstrated the conditionability and potential mechanisms of conditioned immune responses in healthy humans, and (3) investigated conditioned immunomodulation in a clinical sample. Together, these data demonstrate that animal models provide a basis for investigating mechanisms whereby conditioned changes in immune function may modulate health status in a clinical realm.</abstract>
<note type="content">Fig. 1: Conditioned immunomodulation in the rat: conditioning paradigm and experimental groups. Animals received three CS-UCS pairings, followed by three CS reexposures. Animals were sacrificed one hour following the third CS reexposure, with blood and organs removed for immunological analysis.</note>
<note type="content">Fig. 2: Conditioning produces a reduction in splenocyte proliferation (A) and IL-2 production (B) which approaches that effected by cyclosporin administration. Surgical denervation of the spleen blocks the reduced proliferation and cytokine production in conditioned animals, but not in cyclosporin treated rats (C and D). **P<0.01, ***P<0.001.</note>
<note type="content">Fig. 3: (A) Conditioning prolongs the survival time of heart allografts in the rat to a similar magnitude as that achieved by short-course CsA treatment. (B) The addition of sub-therapeutic CsA regime to each group further improves graft survival in conditioned animals only. Importantly, the combination of conditioning and sub-therapeutic CsA therapy produced long-term survival (>100 days) in 20% of animals. Furthermore, the conditioned prolongation of graft survival was completely blocked by prior surgical denervation of the spleen.</note>
<note type="content">Fig. 4: Modulation of NK cell activity (NKCA, in % lysis; effector:target ratio=50:1) in the conditioned group (CS+), UCS control group (UCS), unpaired control group (NC) and saline control group (Sal) five min before and 20 min following CS reexposure (*P<0.05).</note>
<note type="content">Fig. 5: Modulation of the percentage of NK cells following presentation of the CS+ and CS− on acquisition day 3 and 8 (A) and on test days 11, 12 and 13 (B). *P<0.05; **P<0.01.</note>
<note type="content">Fig. 6: Study paradigm. Cycle A and Cycle B represent two consecutive chemotherapeutic cycles. ANV was measured on 2 days (day −2, day −1) prior to the start of a chemotherapeutic cycle. The chemotherapy cycle commenced on day 0. PNV was monitored over 2 days (day +1, day +2) following completion of the cycle. Blood was drawn in cycle B at day −2 (home environment) and at day 0 (hospital) prior to infusion onset. CS, conditioned stimulus; UCS, unconditioned stimulus.</note>
<note type="content">Table 1: Experimental protocol for the conditioning of NK cell activity in healthy humansa</note>
<note type="content">Table 2: Inclusion criteria for conditioning in pediatric cancer patients</note>
<note type="content">Table 3: NK cell activity (NKCA) and plasma cytokine (IFN-γ, IL-1β) concentrations in ANV+ and ANV− patients, measured in the home and in hospital</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>Behavioral conditioning</topic>
<topic>Psychoneuroimmunology</topic>
<topic>Rat</topic>
<topic>Human</topic>
<topic>Sympathetic nervous system</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Behavioural Brain Research</title>
</titleInfo>
<titleInfo type="abbreviated">
<title>BBR</title>
</titleInfo>
<genre type="journal">journal</genre>
<originInfo>
<dateIssued encoding="w3cdtf">200006</dateIssued>
</originInfo>
<identifier type="ISSN">0166-4328</identifier>
<identifier type="PII">S0166-4328(00)X0063-0</identifier>
<part>
<date>200006</date>
<detail type="volume">
<number>110</number>
<caption>vol.</caption>
</detail>
<detail type="issue">
<number>1–2</number>
<caption>no.</caption>
</detail>
<extent unit="issue pages">
<start>1</start>
<end>188</end>
</extent>
<extent unit="pages">
<start>129</start>
<end>141</end>
</extent>
</part>
</relatedItem>
<identifier type="istex">1461CF819CB8832BA9C0AB1104B0F9386F240C89</identifier>
<identifier type="DOI">10.1016/S0166-4328(99)00191-6</identifier>
<identifier type="PII">S0166-4328(99)00191-6</identifier>
<accessCondition type="use and reproduction" contentType="copyright">©2000 Elsevier Science B.V.</accessCondition>
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<recordContentSource>ELSEVIER</recordContentSource>
<recordOrigin>Elsevier Science B.V., ©2000</recordOrigin>
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