The Adhesion, Migration and Chemotaxis of Leucocytes in Inflammation

Wilkinson, P. C.; Lackie, J. M.

doi:10.1007/978-3-642-67311-5_3

Cited by 45 publications

(19 citation statements)

References 171 publications

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“…Enhanced polymorphonuclear leukocyte (PMN) margination characteristically occurs at sites of acute inflammation, whereas monocyte interactions with the microvasculature are observed more often in chronic inflammatory reactions (1)(2)(3)(4)(5). Focal attachment of monocytes to the endothelium also occurs in large arteries as an early event in the development of atherosclerotic lesions (6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

“…Recent in vitro studies with cultured vascular endothelium have provided new insights into the effects of inflammatory mediators on endothelial-leukocyte interactions (4,5,10). In particular, it has been shown that chemotactic factors, such as purified complement components, formyl-methionyl-leucyl-phenylalanine and leukotriene B4, can augment the attachment of PMN to cultured endothelial monolayers (1 1-18).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines.

Bevilacqua¹,

Pober²,

Wheeler³

et al. 1985

J. Clin. Invest.

1,031

369

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Increased leukocyte adhesion to the endothelial lining of blood vessels is an essential event in inflammation and the pathogenesis of certain vascular diseases. We have studied the effect of interleukin 1 (IL-1), an inflammatory/immune mediator, on endothelial-leukocyte adhesion using quantitative in vitro assays. Selective pretreatment of cultured human umbilical vein endothelial monolayers with IL-1 (5 U/ml, 4 h) resulted in an 18.3±2.6-fold increase in human peripheral blood polymorphonuclear leukocyte (PMN) adhesion (mean±SEM, n = 16) and a 2.6±0.3-fold increase in monocyte adhesion (n = 7) over basal levels. IL-i-treated endothelial monolayers also supported increased adhesion of the promyelocytic cell line HL-60 and the monocytelike cell line U937 (33.0±6.0-fold, n = 6 and 4.9±0.5-fold, n = 15, respectively). In contrast, selective IL-1 pretreatment of leukocytes, or the addition of IL-1 during the adhesion assay, did not alter endothelial-leukocyte adhesion. Conditioned medium from IL-i-treated endothelial cultures also did not promote leukocyte adhesion to untreated monolayers. IL-i induction of endothelial adhesivity was concentration dependent (maximum, 10 U/ml), time dependent (peak, 4-6 h), and reversible, was blocked by cycloheximide (10 gg/ml) or actinomycin D (5 ,gg/ml) but not by acetylsalicylic acid (100 .M), and occurred without detectable endothelial cell damage. IL-1 treatment of SV40-transformed human endothelial cells and dermal fibroblasts did not increase their adhesivity for leukocytes. These data suggest that IL-1 can act selectively on human vascular endothelium to increase its adhesivity for circulating blood leukocytes, and thus to localize leukocyte-vessel wall interactions at sites of inflammation in vivo.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines.

Bevilacqua¹,

Pober²,

Wheeler³

et al. 1985

J. Clin. Invest.

1,031

369

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“…Although neutrophil adhesion and emigration have been studied extensively (1)(2)(3)(4), the mechanisms by which neutrophils recognize and adhere to endothelial cells and subsequently migrate through interendothelial cell junctions are still not understood.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil-endothelial cell interactions. Modulation of neutrophil adhesiveness induced by complement fragments C5a and C5a des arg and formyl-methionyl-leucyl-phenylalanine in vitro.

Tonnesen¹,

Smedly²,

Henson³

1984

J. Clin. Invest.

226

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(FMLP), in concentrations ranging from 10-10 to 10-6 M, increased neutrophil adherence to endothelium in a dose-dependent manner. Purified C5a and C5a des arg were essentially equal in their ability to enhance neutrophil adherence, in contrast to the previously described greater in vitro potency of C5a compared with C5a des arg in stimulating neutrophil chemotaxis and enzyme release. Nonstimulated neutrophils adhered preferentially to human endothelial cells compared with fibroblasts or smooth muscle cells, sug-

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“…Neutrophil migration through a 3 -p pore-size membrane filter is affected by several factors, such as deformability (15)(16)(17)(18) of the cells and their adhesiveness to the filter substance (19). Immunoglobulin G is one of the cell-directed inhibitors in normal human serum and increases adherence of neutrophils to nylon fibers (20), whereas chemotactic factors increase deformability of these cells (21).…”

Section: Discussionmentioning

confidence: 99%

Chemotaxis in yersinia arthritis.

Repo¹,

Leirisalo²,

Tiilikainen³

et al. 1982

Arthritis & Rheumatism

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Chemotactic and chemokinetic migration of polymorphonuclear leukocytes in sera from patients with previous yersinia arthritis and from healthy subjects with or without HLA-B27 were studied by the leading front method. Irrespective of yersinia arthritis, zymosan-activated sera from subjects who were HLA-B27 positive were significantly more chemokinetic than were HLA-B27 negative zymosan-activated sera from healthy control subjects. The chemotactic activities of zymosan-activated sera that were HLA-B27 positive or negative, as determined by chemotactic increments, were much the same. The results suggest that zymosanactivated serum that is HLA-B27 positive stimulates random migration of polymorphonuciear leukocytes, but not their directional migration, more than does HLA-B27 negative serum that has been zymosan activated. This may contribute to accumulation of polymorphonuclear leukocytes at the site of inflammation in vivo and thereby to inflammatory symptoms in yersinia arthritis patients with HLA-B27.

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The Adhesion, Migration and Chemotaxis of Leucocytes in Inflammation

Cited by 45 publications

References 171 publications

Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines.

Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines.

Neutrophil-endothelial cell interactions. Modulation of neutrophil adhesiveness induced by complement fragments C5a and C5a des arg and formyl-methionyl-leucyl-phenylalanine in vitro.

Chemotaxis in yersinia arthritis.

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