Document Detail

Human alveolar macrophages and monocytes as a source and target for nitric oxide.
MedLine Citation:
PMID:  11515813     Owner:  NLM     Status:  MEDLINE    
Nitric oxide (NO) is synthesized in the lung and this free radical participates in a wide array of regulatory, protective, and adverse interactions with cells. Both excess NO and its insufficiency have been implicated in the pathogenesis of numerous lung diseases with inflammatory components. Much of the available data concerning the source and regulation of NO production is derived from rodent systems. However, the requirements for NO production are more stringent in human monocytes/macrophages than in rodent systems. In contrast to rodent macrophages, human moncytes/macrophages generally do not respond to cytokine triggers with NO production [J. Leukocyte Biol. 58 (1995) 643, J. Exp. Med. 181 (1995) 735] and if NO is detected the levels are generally low [J. Leukocyte Biol. 58 (1995) 643]. The regulation of macrophage NO in the human appears to be a more selective and variable process than that seen in the rodent macrophages. In the human lung, the function of NO as toxic pro-inflammatory or protective anti-inflammatory agent is unresolved. While not a major source of NO in the human lung, the alveolar macrophage is an important producer of cytokines and this production may be modified by NO. Clear evidence of abnormalities in NO levels in the lungs of patients with asthma, bronchiectasis, viral infections, lung cancer and primary pulmonary hypertension (PPH) has been documented. Elevated inflammatory cytokines and oxidant production have been associated with all of these disease states. In terms of cytokine production, NO has been shown to decrease nuclear factor kappa B (NF-kappaB) activation. However, oxidants may interact with NO to form toxic compounds (e.g., NO combines with superoxide anion to form peroxynitrite). Furthermore, such reactions may decrease the availability of NO for blocking inflammatory cytokine production. Thus, available data suggests that a multiplicity of factors affect NO regulatory properties in inflammatory situations.
M J Thomassen; M S Kavuru
Related Documents :
2192913 - Inhibition of lung damage caused by paraquat with lymphokines or cytokines.
3026723 - Immunopharmacology of anaphylatoxin-induced bronchoconstrictor responses.
23544153 - The alkaloid compound harmane increases the lifespan of caenorhabditis elegans during b...
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  International immunopharmacology     Volume:  1     ISSN:  1567-5769     ISO Abbreviation:  Int. Immunopharmacol.     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-08-22     Completed Date:  2002-01-22     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  100965259     Medline TA:  Int Immunopharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1479-90     Citation Subset:  IM    
Department of Pulmonary and Critical Care Medicine, Cleveland Clinic Foundation, OH 44195-5038, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Macrophages, Alveolar / immunology,  metabolism*
Monocytes / immunology,  metabolism*
Nitric Oxide / physiology*
Reg. No./Substance:
10102-43-9/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  The role of NO in contact hypersensitivity.
Next Document:  Nitric oxide and T helper cell immunity.