scholarly journals Mast Cell Adhesion to Extracellular Matrix: Local Effects of Acute Phase Reactants

1997 ◽  
Vol 113 (1-3) ◽  
pp. 295-296 ◽  
Author(s):  
Rami Hershkoviz ◽  
Liana Preciado-Patt ◽  
Ofer Lider ◽  
Mati Fridkin ◽  
Yoseph A. Mekori
Keyword(s):  
Extracellular Matrix ◽  
Mast Cell ◽  
Cell Adhesion ◽  
Acute Phase ◽  
Local Effects ◽  
Acute Phase Reactants

Regulatory effects of stem cell factor and interleukin-4 on adhesion of human mast cells to extracellular matrix proteins

Blood ◽  
2002 ◽  
Vol 99 (3) ◽  
pp. 966-972 ◽  
Author(s):  
Axel Lorentz ◽  
Detlef Schuppan ◽  
Andreas Gebert ◽  
Michael P. Manns ◽  
Stephan C. Bischoff
Keyword(s):  
Extracellular Matrix ◽  
Mast Cell ◽  
Stem Cell ◽  
Cell Adhesion ◽  
Mast Cells ◽  
Stem Cell Factor ◽  
Collagen I ◽  
Interleukin 4 ◽  
Human Mast Cells ◽  
Ecm Proteins

Abstract Mast cells are inflammatory and immunoregulatory cells resident in tissues. They develop from bone marrow-derived progenitor cells that enter the tissue through the blood circulation. The specific localization and migration of mast cells in tissues is dependent on their interaction with extracellular matrix (ECM) proteins. Adhesion of human mast cells isolated from intestinal mucosa and cultured in the presence of stem cell factor (SCF) to ECM proteins is analyzed. It was observed that SCF is a unique cytokine enhancing mast cell adhesion to all tested ECM proteins (fibronectin, laminin, collagen I, III, IV, VI, XIV) up to 5-fold, particularly to fibronectin (54% ± 12% of mast cells) and to denatured collagens (40% ± 12% on cyanogen bromide-cleaved peptides of collagen I). Most noteworthy, preculture of mast cells with interleukin-4 (IL-4), in addition to SCF, reduced their potency to adhere to ECM proteins to one third compared to mast cells cultured with SCF alone. Mast cell adhesion was preferentially mediated by β1 integrins, and most cells expressed the ECM-binding integrins α2β1, α3β1, α4β1, α5β1, and αVβ3. SCF-induced mast cell adhesion was totally blocked by wortmannin and apigenin, indicating an involvement of phosphatidylinositol 3-kinase and mitogen-activated protein kinase, and it was related to an up-regulation of the HUTS-21 β1 epitope, which is associated with an activated conformation of β1. In conclusion, these data indicate that SCF induces the adhesion of cultured mast cells to ECM proteins, whereas IL-4 may promote detachment from the ECM.

scholarly journals Hypoxia modulates human mast cell adhesion to hyaluronic acid

2021 ◽  
Author(s):  
Joanna Pastwińska ◽  
Aurelia Walczak-Drzewiecka ◽  
Elżbieta Kozłowska ◽  
Enjuro Harunari ◽  
Marcin Ratajewski ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mast Cell ◽  
Hyaluronic Acid ◽  
Cell Adhesion ◽  
Mast Cells ◽  
Immune Cell ◽  
Human Mast Cell ◽  
Dependent Manner ◽  
Cell Functions ◽  
Extracellular Matrix Components

AbstractHypoxia is an inherent factor in the inflammatory process and is important in the regulation of some immune cell functions, including the expression of mast cell pro- and anti-inflammatory mediators. Hypoxia also influences cell adhesion to the extracellular matrix (ECM). Hyaluronic acid is one of the major components of the ECM that is involved in inflammatory and tissue regeneration processes in which mast cells play a prominent role. This prompted us to investigate the effects of hypoxia on the expression of hyaluronic acid receptors in mast cells and mast cell adhesion to this ECM component. We found that human LAD2 mast cells spontaneously adhered to hyaluronic acid in a CD44-dependent manner and that reduced oxygen concentrations inhibited or even completely abolished this adhesion process. The mechanism of hypoxia downregulation of mast cell adhesion to hyaluronic acid did not involve a decrease in CD44 expression and hyaluronidase-mediated degradation of adhesion substrates but rather conformational changes in the avidity of CD44 to hyaluronic acid. Hypoxia-mediated regulation of mast cell adhesion to extracellular matrix components might be involved in the pathogenic accumulation of mast cells observed in the course of certain diseases including rheumatoid arthritis and cancer.

Extracellular matrix-anchored serum amyloid A preferentially induces mast cell adhesion

1997 ◽  
Vol 273 (1) ◽  
pp. C179-C187 ◽  
Author(s):  
R. Hershkoviz ◽  
L. Preciado-Patt ◽  
O. Lider ◽  
M. Fridkin ◽  
J. Dastych ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mast Cell ◽  
Cell Adhesion ◽  
Amino Acid ◽  
Mast Cells ◽  
Serum Amyloid A ◽  
Immune Cell ◽  
Serum Amyloid ◽  
Amino Acid Residues ◽  
Amyloid A

Mast cells are known to accumulate in various inflammatory processes, some of which are known to be associated with increased local and systemic levels of acute-phase reactants such as serum amyloid A (SAA) or with amyloid deposition. The mechanism(s) by which mast cells are recruited to these sites, however, has not been fully elucidated. It has recently been shown that SAA interacts with extracellular matrix (ECM) components and thereby acts as a chemoattractant and regulator of immune cell migration. On the basis of these observations, we examined the effect of SAA on mast cell adhesion to ECM, an essential step in cellular transmigration. We could first demonstrate strong specific binding of recombinant human SAA (rSAA) to murine mast cells using flow cytometry. Moreover, radiolabeled rSAA was found to bind, in a saturable manner, to mast cells, reaching a binding affinity of 10(-8) M. When immobilized by preincubation with ECM, SAA or its proteolytically degraded amyloid A fragment (amino acid residues 2-82), which contains RGD-related adhesion motif but not the COOH-terminal portion of SAA (amino acid residues 77-104), induced the adhesion of resting mast cells to ECM or laminin. SAA and AA, in soluble or immobilized forms, did not activate mast cells to release mediators. Mast cell adhesion to the immobilized ECM-SAA complex appeared to occur through an integrin recognition, inasmuch as adhesion was calcium dependent and could be blocked by an RGD-containing peptide or by anti-CD29 monoclonal antibody. Genistein also inhibited adhesion, indicating that tyrosine kinase activity was involved. These data suggest that SAA bound to ECM may serve as an important inducer of mast cell adhesion, thus regulating mast cell recruitment and accumulation at these sites, which in turn could potentiate further pathology.

Inhibition of T cell adhesion to extracellular matrix glycoproteins by histamine: a role for mast cell degranulation products

1994 ◽  
Vol 56 (4) ◽  
pp. 495-501 ◽  
Author(s):  
Rami Hershkoviz ◽  
Ofer Lider ◽  
Dana Baram ◽  
Tamar Reshef ◽  
Shmuel Miron ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mast Cell ◽  
Cell Adhesion ◽  
T Cell ◽  
Mast Cell Degranulation ◽  
T Cell Adhesion

Tests for Platelet Changes, Acute Phase Reactants and Serum Lipids in Diabetes mellitus and Peripheral Vascular Disease

1982 ◽  
Vol 48 (03) ◽  
pp. 289-293 ◽  
Author(s):  
B A van Oost ◽  
B F E Veldhuyzen ◽  
H C van Houwelingen ◽  
A P M Timmermans ◽  
J J Sixma
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Acute Phase ◽  
Serum Lipids ◽  
Diabetic Patients ◽  
Peripheral Vascular ◽  
Acute Phase Reactants ◽  
Control Subjects ◽  
And Control

SummaryPlatelets tests, acute phase reactants and serum lipids were measured in patients with diabetes mellitus and patients with peripheral vascular disease. Patients frequently had abnormal platelet tests and significantly increased acute phase reactants and serum lipids, compared to young healthy control subjects. These differences were compared with multidiscriminant analysis. Patients could be separated in part from the control subjects with variables derived from the measurement of acute phase proteins and serum lipids. Platelet test results improved the separation between diabetics and control subjects, but not between patients with peripheral vascular disease and control subjects. Diabetic patients with severe retinopathy frequently had evidence of platelet activation. They also had increased acute phase reactants and serum lipids compared to diabetics with absent or nonproliferative retinopathy. In patients with peripheral vascular disease, only the fibrinogen concentration was related to the degree of vessel damage by arteriography.

A Study of Serum Copper and Certain "Acute-Phase Reactants" in Alcoholics

1961 ◽  
Vol 22 (4) ◽  
pp. 544-549 ◽  
Author(s):  
Eugene W. Rice ◽  
Robert E. Olson ◽  
Paul D. Sweeney
Keyword(s):  
Acute Phase ◽  
Serum Copper ◽  
Acute Phase Reactants
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