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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1998-8-26
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pubmed:abstractText |
Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signaling, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previous findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treated with NT (0.5 mg/day/kg body weight) have a depressed inflammatory response in the turpentine-induced abscess model of inflammation. This ability of nicotine to attenuate an inflammatory response may also be the cause of reduced mortality of chronically nicotine-treated mice from acute influenza A pneumonitis. Moreover, in LEW rats, decreased anti-SRBC AFC responses were also observed after intracerebroventricular (i.c.v.) administration of relatively small concentrations of NT (28 micrograms/day/kg body weight) which, when given peripherally, did not affect the AFC response. In vitro the addition of NT to T cells increased protein tyrosine kinase (PTK) activity and intracellular Ca2+ concentration [Ca2+]i. These results support the hypothesis that NT alters immune responses by directly interacting with T cells, as well as indirectly through brain-immune interactions.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Nicotine,
http://linkedlifedata.com/resource/pubmed/chemical/Nicotinic Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0306-4530
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
189-204
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:9621398-Abscess,
pubmed-meshheading:9621398-Animals,
pubmed-meshheading:9621398-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:9621398-Body Temperature,
pubmed-meshheading:9621398-Calcium,
pubmed-meshheading:9621398-Hemolytic Plaque Technique,
pubmed-meshheading:9621398-Immune System,
pubmed-meshheading:9621398-Immunity,
pubmed-meshheading:9621398-Influenza A virus,
pubmed-meshheading:9621398-Injections, Intraventricular,
pubmed-meshheading:9621398-Male,
pubmed-meshheading:9621398-Mice,
pubmed-meshheading:9621398-Motor Activity,
pubmed-meshheading:9621398-Nicotine,
pubmed-meshheading:9621398-Nicotinic Agonists,
pubmed-meshheading:9621398-Orthomyxoviridae Infections,
pubmed-meshheading:9621398-Protein-Tyrosine Kinases,
pubmed-meshheading:9621398-Rats,
pubmed-meshheading:9621398-Rats, Inbred Lew,
pubmed-meshheading:9621398-T-Lymphocytes
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pubmed:year |
1998
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pubmed:articleTitle |
Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms.
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pubmed:affiliation |
Division of Pathophysiology, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. msopori@LRRI.org
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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