Linked Life Data

11714820

Source:http://linkedlifedata.com/resource/pubmed/id/11714820

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-11-20
pubmed:abstractText
Although nicotine is thought to be one of the major immunomodulatory components of cigarette smoking, how nicotine alters the host defense of the lung and, in particular, immune responses of alveolar macrophages, which are critical effector cells in the lung defense to infection, is poorly understood. Nicotinic acetylcholine receptors (nAChRs) are the receptor for nicotine and may be involved in the modulation of macrophage function by nicotine. In this study, therefore, nicotine-induced suppression of antimicrobial activity and cytokine responses of alveolar macrophages mediated by nAChRs to Legionella pneumophila, a causative agent for pneumonia, were examined. The murine MH-S alveolar macrophage cell line cells expressed the messages for alpha4 and beta2 subunits of nAChRs, but not alpha7 subunits, determined by RT-PCR. The nicotine treatment of MH-S alveolar macrophages after infection with L. pneumophila significantly enhanced the replication of bacteria in the macrophages and selectively down-regulated the production of IL-6, IL-12, and TNF-alpha, but not IL-10, induced by infection. These effects were completely blocked by a nonselective antagonist, d-tubocurarine, for nAChRs, but not by a selective antagonist, alpha-bungarotoxin, for alpha7-nAChRs. Furthermore, the stimulation of nAChRs with another agonist, 1,1-dimethyl-4-phenylpiperazinium iodide, showed the same effects, which were blocked by the antagonist d-tubocurarine, on the bacterial replication and cytokine regulation with that of nicotine. Thus, the results revealed that nAChRs, the major exogenous ligands of which are nicotine, are involved in the regulation of macrophage immune function by nicotine and may contribute to the cigarette-induced risk factors for respiratory infections in smokers.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
167
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6518-24
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11714820-Adjuvants, Immunologic, pubmed-meshheading:11714820-Animals, pubmed-meshheading:11714820-Anti-Bacterial Agents, pubmed-meshheading:11714820-Bungarotoxins, pubmed-meshheading:11714820-Cell Line, pubmed-meshheading:11714820-Cell Survival, pubmed-meshheading:11714820-Cells, Cultured, pubmed-meshheading:11714820-Cytokines, pubmed-meshheading:11714820-Dimethylphenylpiperazinium Iodide, pubmed-meshheading:11714820-Legionella pneumophila, pubmed-meshheading:11714820-Macrophages, Alveolar, pubmed-meshheading:11714820-Mice, pubmed-meshheading:11714820-Nicotine, pubmed-meshheading:11714820-Nicotinic Agonists, pubmed-meshheading:11714820-Nicotinic Antagonists, pubmed-meshheading:11714820-RNA, Messenger, pubmed-meshheading:11714820-Receptors, Nicotinic, pubmed-meshheading:11714820-Tubocurarine
pubmed:year
2001
pubmed:articleTitle
Involvement of nicotinic acetylcholine receptors in suppression of antimicrobial activity and cytokine responses of alveolar macrophages to Legionella pneumophila infection by nicotine.
pubmed:affiliation
Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't