Linked Life Data

9666281

Source:http://linkedlifedata.com/resource/pubmed/id/9666281

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1998-10-8
pubmed:abstractText
Tobacco smoking may predispose humans to respiratory disease, and may be a compounding risk factor in HIV infection and progression to AIDS. We have demonstrated that chronic exposure of mice and rats to cigarette smoke or nicotine inhibits T cell responsiveness, which may account for the decreased antibody response to T-dependent antigens seen in these animals. This inhibition may result from aberrant antigen-mediated signaling and depletion of IP3-sensitive Ca2+ stores in nicotine-treated animals. Moreover, nicotine appears to moderate the inflammation associated with turpentine-induced sterile abscess and influenza infection. These anti-inflammatory properties of nicotine may account for longer survival of nicotine-treated than control mice lethally infected with influenza virus. However, because inflammation is required for clearance of many pathogens, nicotine-treated mice exhibit significantly higher titers of influenza virus following infection. These results offer an explanation for the higher susceptibility to some infectious diseases, but greater resistance to some inflammatory diseases among human smokers.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
437
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
279-89
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Nicotine-induced modulation of T Cell function. Implications for inflammation and infection.
pubmed:affiliation
Pathophysiology Division, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.