Document Detail


Chemotaxis of alveolar macrophages in response to signals derived from alveolar epithelial cells.
MedLine Citation:
PMID:  9605106     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have postulated that alveolar epithelial cells (AEC) play a critical role in local regulation of alveolar macrophage (AM) recruitment and activation for host defense in the lung. The present study explores the effects of conditioned medium from AEC (AEC-CM) on the migration of AM, using a Boyden chamber assay. AEC-CM was chemotactic for AM, with peak activity observed with a 1:10 dilution. We previously showed that rat AEC express the chemokines RANTES (regulated on activation, normal T expressed and secreted) and monocyte chemoattractant protein 1 (MCP-1) as well as granulocyte-macrophage colony-stimulating factor (GM-CSF). Neutralizing antibodies to RANTES and to MCP-1 and immunoprecipitation of GM-CSF decreased the chemotactic activity of AEC-CM by 58%, 29%, and 47%, respectively. Similar levels of chemotaxis were found in response to recombinant RANTES, MCP-1, and GM-CSF. In each instance the optimal dose was very low (0.01 to 0.1 ng/ml), with diminished chemotaxis at higher doses. Peritoneal macrophages (PM) also migrated in response to AEC-CM and each of the recombinant cytokines; however, AM were much more sensitive to AEC-CM, RANTES, and GM-CSF than were PM. AM migrated preferentially from medium conditioned by unstimulated AEC toward supernatants from interleukin 1alpha-stimulated AEC. Therefore, AEC may control the distribution of AM through the creation of local chemotactic gradients and are likely to play a critical role in the host response to low-level antigen entry into the peripheral lung.
Authors:
A D O'Brien; T J Standiford; P J Christensen; S E Wilcoxen; R Paine
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of laboratory and clinical medicine     Volume:  131     ISSN:  0022-2143     ISO Abbreviation:  J. Lab. Clin. Med.     Publication Date:  1998 May 
Date Detail:
Created Date:  1998-06-19     Completed Date:  1998-06-19     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0375375     Medline TA:  J Lab Clin Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  417-24     Citation Subset:  AIM; IM    
Affiliation:
Department of Internal Medicine, University of Michigan, and the Veterans Affairs Medical Center, Ann Arbor, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / immunology,  pharmacology
Cell Movement / physiology
Chemokine CCL2 / immunology,  pharmacology
Chemokine CCL5 / immunology,  pharmacology
Chemotactic Factors / pharmacology
Chemotaxis / drug effects,  physiology*
Culture Media, Conditioned / pharmacology
Epithelial Cells / physiology*
Granulocyte-Macrophage Colony-Stimulating Factor / immunology,  physiology
Macrophages, Alveolar / drug effects,  physiology*
Macrophages, Peritoneal / drug effects
Male
Pulmonary Alveoli / cytology,  physiology*
Rats
Rats, Sprague-Dawley
Signal Transduction* / physiology
Grant Support
ID/Acronym/Agency:
1P50HL46487/HL/NHLBI NIH HHS; HL50496/HL/NHLBI NIH HHS; HL58200/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies; 0/Chemokine CCL2; 0/Chemokine CCL5; 0/Chemotactic Factors; 0/Culture Media, Conditioned; 83869-56-1/Granulocyte-Macrophage Colony-Stimulating Factor
Comments/Corrections
Comment In:
J Lab Clin Med. 1998 May;131(5):391-2   [PMID:  9605102 ]

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


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