Document Detail


LFA-1 and Mac-1 define characteristically different intralumenal crawling and emigration patterns for monocytes and neutrophils in situ.
MedLine Citation:
PMID:  21037096     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To exit blood vessels, most (∼80%) of the lumenally adhered monocytes and neutrophils crawl toward locations that support transmigration. Using intravital confocal microscopy of anesthetized mouse cremaster muscle, we separately examined the crawling and emigration patterns of monocytes and neutrophils in blood-perfused unstimulated or TNF-α-activated venules. Most of the interacting cells in microvessels are neutrophils; however, in unstimulated venules, a greater percentage of the total monocyte population is adherent compared with neutrophils (58.2 ± 6.1% versus 13.6 ± 0.9%, adhered/total interacting), and they crawl for significantly longer distances (147.3 ± 13.4 versus 61.8 ± 5.4 μm). Intriguingly, after TNF-α activation, monocytes crawled for significantly shorter distances (67.4 ± 9.6 μm), resembling neutrophil crawling. Using function-blocking Abs, we show that these different crawling patterns were due to CD11a/CD18 (LFA-1)- versus CD11b/CD18 (Mac-1)-mediated crawling. Blockade of either Mac-1 or LFA-1 revealed that both LFA-1 and Mac-1 contribute to monocyte crawling; however, the LFA-1-dependent crawling in unstimulated venules becomes Mac-1 dependent upon inflammation, likely due to increased expression of Mac-1. Mac-1 alone was responsible for neutrophil crawling in both unstimulated and TNF-α-activated venules. Consistent with the role of Mac-1 in crawling, Mac-1 block (compared with LFA-1) was also significantly more efficient in blocking TNF-α-induced extravasation of both monocytes and neutrophils in cremaster tissue and the peritoneal cavity. Thus, mechanisms underlying leukocyte crawling are important in regulating the inflammatory responses by regulating the numbers of leukocytes that transmigrate.
Authors:
Ronen Sumagin; Hen Prizant; Elena Lomakina; Richard E Waugh; Ingrid H Sarelius
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-29
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-18     Completed Date:  2011-01-10     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  7057-66     Citation Subset:  AIM; IM    
Affiliation:
Department of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies, Blocking / pharmacology
Antigens, CD18 / physiology
Cell Movement / immunology*
Flow Cytometry
Inflammation Mediators / metabolism,  physiology
Leukocyte Count
Lymphocyte Function-Associated Antigen-1 / biosynthesis,  immunology,  physiology*
Macrophage-1 Antigen / biosynthesis,  immunology,  physiology*
Male
Mice
Mice, Inbred C57BL
Microscopy, Confocal
Microscopy, Fluorescence
Monocytes / immunology*,  metabolism,  ultrastructure
Neutrophil Activation / immunology
Neutrophils / immunology*,  metabolism,  ultrastructure
Tumor Necrosis Factor-alpha / administration & dosage
Venules / immunology,  metabolism,  ultrastructure
Grant Support
ID/Acronym/Agency:
P01 HL018208-34A1/HL/NHLBI NIH HHS; P01 HL18208/HL/NHLBI NIH HHS; R01 HL075186-04/HL/NHLBI NIH HHS; R01 HL75186/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Blocking; 0/Antigens, CD18; 0/Inflammation Mediators; 0/Lymphocyte Function-Associated Antigen-1; 0/Macrophage-1 Antigen; 0/Tumor Necrosis Factor-alpha

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