Interleukin-1 and tumour necrosis factor α induced polymorphonuclear leukocyte-endothelial cell adhesion and transendothelial migration in vitro: the effect of apical versus basal monolayer stimulation

Morzycki, W.; Sadowska, Joanna; Issekutz, Andrew C.

doi:10.1016/0165-2478(90)90204-4

Cited by 45 publications

(31 citation statements)

References 21 publications

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“…1 Endothelial cell dependent IL-ia-induced monocyte migration. In the case of PMNL, activation ofthe HUVE by IL-I or TNF-a induces strong PMNL adhesion and marked transendothelial migration (25-35% of added PMNL) in this assay system as shown by us previously (12). As shown in Fig.…”

Section: Resultsmentioning

confidence: 78%

“…The filters were first prepared by coating with 0.01% gelatin (37°C, 18 h) followed by application of 3 ,g in 50 Ml water of human fibronectin (Collaborative Research) at 37°C for 2 h. Fibronectin was then replaced by HUVE (2 X 104 cells) from the first or second passage, added above the filter in 0.1 ml growth medium, and 0.6 ml growth medium was added to the lower compartment beneath the filter. The HUVE formed a tight permeability barrier in 5-6 d, and were evaluated for confluence before use by '25I-HSA diffusion as previously described (12).…”

Section: Methodsmentioning

confidence: 99%

“…Platelets were found to band above the 40% Percoll cushion. Monocytes were identified by neutral red and nonspecific esterase staining (50) (52), and cultured on filters as previously described by us (12 Gibco Laboratories). The HUVE were detached using 0.025% trypsin/ 0.01% Versene (MA Bioproducts, Walkerville, MD) and cultured on PVP-free polycarbonate filters bearing 51gm pores in 65-mm di culture plate inserts (Transwell 3415; Costar Corp., Cambridge, MA).…”

Section: Methodsmentioning

confidence: 99%

“…In this process, endothelial cells undergo profound functional alterations and express adhesion molecules for leukocytes. These stimuli do not induce PMNL migration directly, but we and others have shown that IL-1, TNF-a, and LPS activate vascular endothelial cells in vitro to increase PMNL adhesion and transendothelial migration (3,6,(12)(13)(14). This process involves increased surface expression on the endothelial cell of the membrane glycoproteins E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule (VCAM-1) (3,15,16).…”

Section: Introductionmentioning

confidence: 99%

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VLA-4 integrin can mediate CD11/CD18-independent transendothelial migration of human monocytes.

Chuluyan

Issekutz²

1993

J. Clin. Invest.

153

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The migration of human monocytes across unactivated and activated human umbilical vein endothelium (HUVE) in response to chemotactic factors was studied, and the adhesion molecules involved were characterized. Migration of blood monocytes or U937 cell line-derived monocytes across unactivated HUVE induced by C5a, was partially inhibited (by 75%) by mAbs (R15.7 or 60.3) to CD18 of the CD11/CD18 complex on the monocyte. However, when the HUVE was pretreated for 5 h with IL-la (0.1 ng/ml), TNF-a (100 U/ml), or LPS (1 ng/ml), migration induced by C5a was no longer inhibited; i.e., migration became CD18 independent. The monocyte CD18-independent migration was completely blocked by mAbs against a4 or 01 integrin chains of VLA4. This migration was also partially inhibited by mAbs against vascular cell adhesion molecule-i (VCAM-1), a major counter-receptor on HUVE for VLA4, but not by mAbs to E-selectin or intercellular adhesion molecule-i. The significant CD18-independent migration across "unactivated" HUVE was also inhibited by mAbs against a4 or #I chains of VLA4, although mAbs against VCAM-1 did not inhibit under these conditions. Finally, considerable VLA4-dependent transendothelial migration to C5a was also observed with monocytes from a patient with CD18 deficiency (leukocyte adhesion deficiency). These results suggest that (a) there is a major CD18-independent component in monocyte chemotactic factor-dependent migration across activated and unactivated endothelium; (b) that VLA4 integrin on the monocyte has a major role in this migration; and (c) that VCAM-1 on activated endothelium functions as a counter-receptor in this process, but other ligands for VLA4, especially on unactivated endothelium, may also be involved. (J. Clin. Invest. 1993. 92:2768-2777

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Section: Resultsmentioning

confidence: 78%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

VLA-4 integrin can mediate CD11/CD18-independent transendothelial migration of human monocytes.

Chuluyan

Issekutz²

1993

J. Clin. Invest.

153

View full text Add to dashboard Cite

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“…HUVEC (2 ϫ 10 4 cells) from the first or second passage were cultured on 2% gelatin-coated Transwell culture inserts (6.5-mm diameter polycarbonate membranes with 5-mm pores; Costar, Cambridge, MA) according to the method of Morzycki et al (8,46). Endothelial cell culture medium (0.2 ml M199; Life Technologies, Grand Island, NY) supplemented with 20% FCS, 2 mM L-glutamine, penicillin (100 U/ml), streptomycin (100 U/ml) (Life Technologies), endothelial cell growth supplement (20 g/ml; Collaborative Research, Bedford, MA), and heparin sodium (90 g/ml; Sigma, St. Louis, MO) was added to the Transwell inserts only.…”

Section: Endothelial Cell Culturesmentioning

confidence: 99%

Migration of Eosinophils Across Endothelial Cell Monolayers: Interactions Among IL-5, Endothelial-Activating Cytokines, and C-C Chemokines

Shahabuddin

Ponath

Schleimer

2000

The Journal of Immunology

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Eosinophils are the predominant cell type recruited in inflammatory reactions in response to allergen challenge. The mechanisms of selective eosinophil recruitment in allergic reactions are not fully elucidated. In this study, the ability of several C-C chemokines to induce transendothelial migration (TEM) of eosinophils in vitro was assessed. Eotaxin, eotaxin-2, monocyte chemotactic protein (MCP)-4, and RANTES induced eosinophil TEM across unstimulated human umbilical vein endothelial cells (HUVEC) in a concentration-dependent manner with the following rank order of potency: eotaxin ≈ eotaxin-2 > MCP-4 ≈ RANTES. The maximal response induced by eotaxin or eotaxin-2 exceeded that of RANTES or MCP-4. Preincubation of eosinophils with anti-CCR3 Ab (7B11) completely blocked eosinophil TEM induced by eotaxin, MCP-4, and RANTES. Activation of endothelial cells with IL-1β or TNF-α induced concentration-dependent migration of eosinophils, which was enhanced synergistically in the presence of eotaxin and RANTES. Anti-CCR3 also inhibited eotaxin-induced eosinophil TEM across TNF-α-stimulated HUVEC. The ability of eosinophil-active cytokines to potentiate eosinophil TEM was assessed by investigating eotaxin or RANTES-induced eosinophil TEM across resting and IL-1β-stimulated HUVEC in the presence or absence of IL-5. The results showed synergy between IL-5 and the chemokines but not between IL-5 and the endothelial activator IL-1β. Our data suggest that eotaxin, eotaxin-2, MCP-4, and RANTES induce eosinophil TEM via CCR3 with varied potency and efficacy. Activation of HUVEC by IL-1β or TNF-α or priming of eosinophils by IL-5 both promote CCR3-dependent migration of eosinophils from the vasculature in conjunction with CCR3-active chemokines.

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Contribution of CD11a/CD18, CD11b/CD18, ICAM-1 (CD54) and −2 (CD102) to human monocyte migration through endothelium and connective tissue fibroblast barriers

Shang

Issekutz

1998

Eur. J. Immunol.

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Recently we reported that monocyte migration through a barrier of human synovial fibroblasts (HSF) is mediated by the CD11/CD18 (beta2) integrins, and the beta1 integrins VLA-4 and VLA-5 on monocytes. Here we investigated in parallel the role of beta2 integrin family members, LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18) on monocytes, and the immunoglobulin supergene family members, ICAM-1 and ICAM-2 on HSF and on human umbilical vein endothelial cells (HUVEC), in monocyte migration through HSF and HUVEC monolayers. Using function blocking monoclonal antibodies (mAb), when both VLA-4 and VLA-5 on monocytes were blocked, treatment of monocytes with mAb to both LFA-1 and to Mac-1 completely inhibited monocyte migration across HSF barriers, although blocking either of these beta2 integrins alone had no effect on migration, even when VLA-4 and VLA-5 were blocked. This indicates that optimal beta2 integrin-dependent monocyte migration in synovial connective tissue may be mediated by either LFA-1 or Mac-1. Both ICAM-1 and ICAM-2 were constitutively expressed on HSF and on HUVEC, although ICAM-2 was only minimally expressed on HSF. Based on results of mAb blockade, ICAM-1 appeared to be the major ligand for LFA-1-dependent migration through the HSF. In contrast, both ICAM-1 and ICAM-2 mediated LFA-1-dependent monocyte migration through HUVEC. However, neither ICAM-1 nor ICAM-2 was required for Mac-1 -dependent monocyte migration through either cell barrier, indicating that Mac-1 can utilize ligands distinct from ICAM-1 and ICAM-2 on HSF and on HUVEC during monocyte transmigration.

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Interleukin-1 and tumour necrosis factor α induced polymorphonuclear leukocyte-endothelial cell adhesion and transendothelial migration in vitro: the effect of apical versus basal monolayer stimulation

Cited by 45 publications

References 21 publications

VLA-4 integrin can mediate CD11/CD18-independent transendothelial migration of human monocytes.

VLA-4 integrin can mediate CD11/CD18-independent transendothelial migration of human monocytes.

Migration of Eosinophils Across Endothelial Cell Monolayers: Interactions Among IL-5, Endothelial-Activating Cytokines, and C-C Chemokines

Contribution of CD11a/CD18, CD11b/CD18, ICAM-1 (CD54) and −2 (CD102) to human monocyte migration through endothelium and connective tissue fibroblast barriers

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