Serum Inhibitor of C5 Fragment-Mediated Polymorphonuclear Leukocyte Chemotaxis Associated with Chronic Hemodialysis

Goldblum, Simeon E.; Epps, Dennis E. Van; Reed, William P.

doi:10.1172/jci109446

Cited by 33 publications

(11 citation statements)

References 39 publications

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“…Whole peripheral blood from healthy human volunteers was collected into acid citrate dextran (Sigma) solution, and neutrophils were isolated by dextran erythrocyte sedimentation and density gradient centrifugation through Ficoll-Hypaque (Sigma) as previously described (30). Neutrophils were resuspended at 10 7 cells/ml in Hanks' balanced salt solution without divalent cations (HBSS) (Life Technologies, Gaithersburg, MD) and incubated with 5 M calcein AM (Molecular Probes) for 40 min with gentle agitation in the dark (3).…”

Section: That Introduced a Bamhi Restriction Site And A 3ј Reverse Prmentioning

confidence: 99%

Protein tyrosine phosphatase activity regulates endothelial cell-cell interactions, the paracellular pathway, and capillary tube stability

Young

Sui

Kiser

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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. Protein tyrosine phosphatase activity regulates endothelial cell-cell interactions, the paracellular pathway, and capillary tube stability. Am J Physiol Lung Cell Mol Physiol 285: L63-L75, 2003. First published March 7, 2003 10.1152/ajplung.00423.2002-Protein tyrosine phosphorylation is tightly regulated through the actions of both protein tyrosine kinases and protein tyrosine phosphatases. In this study, we demonstrate that protein tyrosine phosphatase inhibition promotes tyrosine phosphorylation of endothelial cell-cell adherens junction proteins, opens an endothelial paracellular pathway, and increases both transendothelial albumin flux and neutrophil migration. Tyrosine phosphatase inhibition with sodium orthovanadate or phenylarsine oxide induced dose-and time-dependent increases in [14 C]bovine serum albumin flux across postconfluent bovine pulmonary artery endothelial cell monolayers. These increases in albumin flux were coincident with actin reorganization and intercellular gap formation in both postconfluent monolayers and preformed endothelial cell capillary tubes. Vanadate (25 M) increased tyrosine phosphorylation of endothelial cell proteins 12-fold within 1 h. Tyrosine phosphorylated proteins were immunolocalized to the intercellular boundaries, and several were identified as the endothelial cell-cell adherens junction proteins, vascular-endothelial cadherin, and ␤-, ␥-, and p120-catenin as well as platelet endothelial cell adhesion molecule-1. Of note, these tyrosine phosphorylation events were not associated with disassem-

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Section: That Introduced a Bamhi Restriction Site And A 3ј Reverse Prmentioning

confidence: 99%

Protein tyrosine phosphatase activity regulates endothelial cell-cell interactions, the paracellular pathway, and capillary tube stability

Young

Sui

Kiser

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Although uremia was reported to possibly be associated with the existence of inhibitory serum factors [18,19], the state of 1,25D deficiency was also possibly relevant to the diminished proliferative response. Reinhardt and Hustmyer [20] reported 1,25D to have an inhibitory effect of mitogen responses in vitro.…”

Section: Discussionmentioning

confidence: 99%

Calcitriol Therapy Modulates the Cellular Immune Responses in Hemodialysis Patients

Tokuda

Kano²,

Meiri³

et al. 2000

Am J Nephrol

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We studied the in vitro and in vivo effects of calcitriol (1,25D) on the cellular immune responses in 19 hemodialysis (HD) patients. In vitro 5-day treatment with 1,25D markedly reduced the HLA-DR expression by peripheral blood CD14⁺ monocytes from both HD patients and normal subjects in a similar fashion. The HLA-DR expression by monocytes and the phorbol myristate acetate (PMA)-induced superoxide production (SOP) by neutrophils were significantly higher in the HD patients than in the normal subjects (p < 0.01 and p < 0.05, respectively). The phagocytic activity in the HD patients was significantly lower than that in the normal subjects (p < 0.05). Moreover, the mitogen response of HD peripheral blood lymphocytes against pokeweed mitogen (PWM) was significantly lower than that of the controls (p < 0.01) but was only slightly and insignificantly lower against Con A. Oral 1,25D pulse therapy resulted in a marked decrease in the HLA-DR expression by peripheral blood monocytes 2 and 4 days after the first 1,25D administration (p < 0.01) in HD patients. Moreover, the treatment significantly enhanced the PMA-induced SOP 2 days after the treatment (p < 0.01). However, the phagocytic activity by neutrophils and the mitogen responses to Con A and PWM by lymphocytes were not significantly affected by this treatment. These results suggest that 1,25D plays a significant role in the regulation of both the monocyte and neutrophil functions in HD patients.

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“…Also, sera from dialysis patients contain a heat-stable factor that inhibited granulocyte chemotaxis [7], The mechanisms and/or the potential uremic factors underly ing these defects in leukocyte functions are not known.…”

Section: Introductionmentioning

confidence: 99%

Effect of Parathyroid Hormone on Random Migration of Human Polymorphonuclear Leukocytes

Doherty¹,

LaBelle²,

Collins³

et al. 1988

Am J Nephrol

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Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1–84 PTH but not its amino-terminal (1–34 PTH) or its carboxy-terminal (53–84 PTH) fragments produced marked and significant (p < 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1–84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p < 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16–20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p < 0.01) reduced and there was a significant (p < 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure. The data show that (1) PMNL are target cells for intact 1–84 PTH; (2) the effect of PTH on PMNL migration is specific to the hormone and is related to its biological activity; (3) this action of the hormone is not mediated by calcium influx into PMNL nor by stimulation of cAMP or cGMP production in these cells but may be due to redistribution of cytosolic calcium between various cell organelles; (4) prolonged exposure to intact PTH may adversely affect random migration of PMNL, and (5) the migration of PMNL is impaired in most patients with chronic renal failure and it is inversely related to serum levels of PTH. The data are consistent with the notion that the state of secondary hyperparathyroidism of chronic renal failure is responsible for altered PMNL migration and assign a new dimension for PTH toxicity in these patients.

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Serum Inhibitor of C5 Fragment-Mediated Polymorphonuclear Leukocyte Chemotaxis Associated with Chronic Hemodialysis

Cited by 33 publications

References 39 publications

Protein tyrosine phosphatase activity regulates endothelial cell-cell interactions, the paracellular pathway, and capillary tube stability

Protein tyrosine phosphatase activity regulates endothelial cell-cell interactions, the paracellular pathway, and capillary tube stability

Calcitriol Therapy Modulates the Cellular Immune Responses in Hemodialysis Patients

Effect of Parathyroid Hormone on Random Migration of Human Polymorphonuclear Leukocytes

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