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Journal articles on the topic 'Polymorphonuclear leukocyte'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Boxer, Grace Jordison, John T. Curnutte, and Laurence A. Boxer. "Polymorphonuclear Leukocyte Function." Hospital Practice 20, no. 3 (1985): 69–90. http://dx.doi.org/10.1080/21548331.1985.11703014.

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2

Wakefield, Christian H. "Polymorphonuclear Leukocyte Activation." Archives of Surgery 128, no. 4 (1993): 390. http://dx.doi.org/10.1001/archsurg.1993.01420160028003.

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3

Hasçelik, G., B. ŞLener, and Z. Hasçelik. "Effect of Some Anti-Inflammatory Drugs on Human Neutrophil Chemotaxis." Journal of International Medical Research 22, no. 2 (1994): 100–106. http://dx.doi.org/10.1177/030006059402200206.

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The effects of piroxicam, tenoxicam, diclofenac sodium, acetylsalicylic acid and tiaprofenic acid on the chemotaxis and random migration of human polymorphonuclear leukocytes were investigated, using zymosan-activated serum as chemo-attractant, with a modified Boyden chamber technique. All five compounds significantly reduced chemotaxis. The random migration of polymorphonuclear leukocytes was inhibited by piroxicam, diclofenac sodium and tiaprofenic acid but not by tenoxicam or acetylsalicylic acid. The inhibitory effect of these non-steroidal anti-inflammatory drugs on polymorphonuclear leukocyte chemotaxis and on random migration was generally dose-dependent. The results suggest that the drugs studied may have a direct effect on polymorphonuclear leukocyte chemotaxis and that this activity may contribute to their anti-inflammatory properties.

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4

Shasby, D. M., S. S. Shasby, and M. J. Peach. "Polymorphonuclear leukocyte: arachidonate edema." Journal of Applied Physiology 59, no. 1 (1985): 47–55. http://dx.doi.org/10.1152/jappl.1985.59.1.47.

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Polymorphonuclear leukocytes (PMN) are important participants in many models of acute lung edema. Enhanced metabolism of arachidonate is also characteristic of many of these models. We found that PMN and arachidonate, but neither alone, increased alveolar capillary permeability of isolated perfused lungs and increased transfer of albumin across monolayers of endothelial cells cultured on micropore filters. Inhibition of PMN, but not endothelial cyclooxygenase, blunted the edematous process. Neither PMN proteases nor PMN-derived oxidants were involved. The edemagenic activity was not found in supernatants of PMN and arachidonate, and unstable prostaglandins did not alter endothelial albumin transfer. The edemagenic process was not inhibited by blocking leukotriene synthesis, and endothelial albumin transfer was not increased by direct addition of leukotrienes to endothelium. These data demonstrate that PMN and arachidonate can interact to increase endothelial permeability and that PMN cyclooxygenase activity is important for this process. This interaction is of potential significance to the acute inflammatory process in the lung vasculature.

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5

Del Maschio, A., V. Evangelista, G. Rajtar, Z. M. Chen, C. Cerletti, and G. De Gaetano. "Platelet activation by polymorphonuclear leukocytes exposed to chemotactic agents." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (1990): H870—H879. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h870.

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Human platelets were loaded with aequorin, a Ca2(+)-sensitive photoprotein, and tested in the platelet-ionized calcium aggregometer for simultaneous recording of platelet aggregation and intraplatelet Ca2+ levels both in the presence and in the absence of autologous polymorphonuclear leukocytes. Cells were exposed to one of three chemotactic stimuli: platelet-activating factor (PAF), N-formyl-methionyl-leucyl-phenylalanine (FMLP), or leukotriene B4 (LTB4). Platelets alone aggregated and showed intracellular Ca2+ movement only when exposed to PAF. Amplification of both platelet aggregation and intraplatelet Ca2+ movement was induced by PAF in the presence of leukocytes. Aggregation and intraplatelet Ca2+ mobilization were also observed in the presence of leukocytes activated by either FMLP or LTB4. Both parameters increased with the concentration of the stimuli and/or the number of leukocytes. Platelet thromboxane B2 production was also significantly increased in the presence of leukocytes. Addition of platelets at different times after leukocyte activation resulted in progressively reduced cytoplasmic Ca2+ increase. Cell-free supernatants prepared from FMLP-stimulated leukocytes were able to induce platelet aggregation, thromboxane B2 generation, and Ca2+ mobilization, although at a reduced degree as compared with intact leukocyte addition. The activity of leukocyte supernatants was stable at 37 degrees C for up to 30 min and was suppressed by trypsin inhibitor. Our study indicates that stimulated leukocytes release a soluble enzymatic activity able to activate platelets; cell-to-cell interaction may also play a role in this phenomenon. Platelet-leukocyte interaction could have physiopathological relevance and constitutes a new model for studying old and new platelet inhibitory drugs.

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6

Goihman-Yahr, Mauricio, Tulio Molina, Blanca San Martin, et al. "Polymorphonuclear Leukocyte Functions in Psoriasis." International Journal of Dermatology 27, no. 9 (1988): 633–37. http://dx.doi.org/10.1111/j.1365-4362.1988.tb02421.x.

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7

Boxer, Grace Jordison, John T. Curnutte, and Laurence A. Boxer. "Disorders of Polymorphonuclear Leukocyte Function." Hospital Practice 20, no. 4 (1985): 129–38. http://dx.doi.org/10.1080/21548331.1985.11703040.

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8

Tanaka, Hirotoshi, Yoichi Ichikawa, Hideto Akama, and Mitsuo Homma. "In vivo responsiveness to glucocorticoid correlated with glucocorticoid receptor content in peripheral blood leukocytes in normal humans." Acta Endocrinologica 121, no. 4 (1989): 470–76. http://dx.doi.org/10.1530/acta.0.1210470.

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Abstract. Dexamethasone loading tests (0.1 mg dexamethasone/kg, iv) were performed in 18 normal males to evaluate the individual responsiveness to glucocorticoid. There were inter-individual differences in increase in peripheral blood polymorphonuclear leukocyte count, decrease in peripheral blood lymphocyte count, and increase in plasma free fatty acids levels after dexamethasone injection. In addition, there was a significant correlation between the maximum increase in polymorphonuclear leukocytes and the maximum decrease in lymphocytes (r = 0.7514, p < 0.0003). Simultaneous measurements of glucocorticoid receptor content by whole-cell assay revealed that glucocorticoid receptor content in polymorphonuclear leukocytes linearly correlated with that in the corresponding lymphocytes (r = 0.9482, p < 0.0001). There were also significant correlations between the maximum increase in polymorphonuclear leukocytes and glucocorticoid receptor content in polymorphonuclear leukocytes (r = 0.7239, p < 0.0007), and between the maximum decrease in lymphocytes and glucocorticoid receptor content in lymphocytes (r = 0.7703, p < 0.0002). These results suggest that individual differences are preserved both in glucocorticoid responsiveness and in glucocorticoid receptor content in peripheral blood leukocytes in normal humans.

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9

Ember, Julia A., Gregory J. del Zoppo, Etsuro Mori, Winston S. Thomas, Brian R. Copeland, and Tony E. Hugli. "Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model." Journal of Cerebral Blood Flow & Metabolism 14, no. 6 (1994): 1046–54. http://dx.doi.org/10.1038/jcbfm.1994.137.

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There is increasing interest in the role of polymorphonuclear (PMN) leukocytes in the evolution of focal cerebral infarction. Surgical preparation of focal cerebral ischemia models may alter leukocyte reactivity and thereby make interpretation of leukocyte function following ischemia/reperfusion difficult. The effects of surgical preparation and of experimental ischemia/reperfusion on granulocyte function have been examined prospectively in a baboon model. Twenty-six adolescent male baboons underwent surgical preparation, of which 21 underwent middle cerebral artery occlusion/reperfusion. Four additional animals served as nonsurgical controls. Peripheral venous blood specimens were taken for performing assays of leukocyte function at defined intervals before and after both the surgical preparation (i.e., the overall procedure for implantation of the middle cerebral artery occlusion device) and occlusion/reperfusion. A stress-related elevation in total leukocyte number was attributed mainly to an increase in the number of circulating PMN leukocytes. Values rose from 13.9 ± 4.9 × 103 to 27.8 ± 5.8 × 103/μl, (±SD; n = 21) for total leukocyte number, with p < 0.001, and from 4.3 ± 2.1 × 103 to 15.9 ± 4.7 × 103/μl ( n = 21) for PMN leukocytes, with p < 0.001. Surgical preparation had no effect ( p ≥ 0.4) on the ability of PMN leukocytes, isolated 24 h after the implantation procedure, to display polarization, O2– production, or β-glucuronidase release when stimulated with human C5a. A moderate decrease in the chemotactic response to C5a resolved within the 7-day postsurgery (preocclusion) period. Three-hour middle cerebral artery occlusion and 1-h reperfusion resulted in a significant reduction in C5a-induced polarization. The preocclusion value of 82 ± 9.7 ( n = 7) was compared with the occlusion/reperfusion value at 58.8 ± 13.7 ( n = 6; p < 0.05). A moderate decrease was observed in C5a-induced O2– and β-glucuronidase release, as well as a decrease in the chemotactic response. In the nonhuman primate model, the reversible alterations (i.e., chemotaxis) in granulocyte function that were noted following surgical preparation resolved within 7 days. In contrast, middle cerebral artery occlusion/reperfusion was associated with a more dramatic and significant reduction in multiple granulocyte functions elicited by the endogenous mediator C5a as observed 1 h postreperfusion.

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10

Pecsvarady, Z., T. C. Fisher, C. H. Darwin, et al. "Decreased Polymorphonuclear Leukocyte Deformability in NIDDM." Diabetes Care 17, no. 1 (1994): 57–63. http://dx.doi.org/10.2337/diacare.17.1.57.

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11

Kira, Jun-ichi. "Description of polymorphonuclear leukocyte in Japanese." Rinsho Shinkeigaku 49, no. 4 (2009): 195. http://dx.doi.org/10.5692/clinicalneurol.49.195.

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12

Hong, Yun Sik. "Polymorphonuclear leukocyte functions enhanced by chemotaxis." Journal of Korean Medical Science 7, no. 4 (1992): 307. http://dx.doi.org/10.3346/jkms.1992.7.4.307.

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13

Kinoshita, Yo, Kiyokazu Masuda, and Yohnosuke Kobayashi. "51-Chromium Labeled Polymorphonuclear Leukocyte Chemotaxis." Journal of Kansai Medical University 38, no. 3 (1986): 364–72. http://dx.doi.org/10.5361/jkmu1956.38.3_364.

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14

Dhôte, Robin, Pascale Dhôte-Burger, Thierry Thevenot, et al. "Polymorphonuclear Leukocyte-elastase in Crohn's Disease." Journal of Clinical Gastroenterology 31, no. 2 (2000): 152–55. http://dx.doi.org/10.1097/00004836-200009000-00013.

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15

Naess, Are, Kristin Stenhaug Kilhus, Tone W. Nystad, and Steinar Sørnes. "Linezolid and Human Polymorphonuclear Leukocyte Function." Chemotherapy 52, no. 3 (2006): 122–24. http://dx.doi.org/10.1159/000092539.

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16

Podikoglou, D. G., P. E. Lianou, C. D. Tsakanikas, and J. Th Papavassiliou. "Polymorphonuclear leukocyte functions and multiple sclerosis." Neurology 44, no. 1 (1994): 129. http://dx.doi.org/10.1212/wnl.44.1.129.

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17

Mayer, M. "Polymorphonuclear leukocyte functions in multiple sclerosis." Neurology 44, no. 11 (1994): 2216. http://dx.doi.org/10.1212/wnl.44.11.2216-b.

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18

Podikoglou, D. G., P. E. Lianou, C. D. Tsakanikas, and J. Th Papavassiliou. "Polymorphonuclear leukocyte functions in multiple sclerosis." Neurology 44, no. 11 (1994): 2217. http://dx.doi.org/10.1212/wnl.44.11.2217.

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19

Caimi, G., B. Canino, F. Ferrara, M. Montana, and R. Lo Presti. "Polymorphonuclear Leukocyte Integrinsin Deep Venous Thrombosis." Clinical and Applied Thrombosis/Hemostasis 11, no. 1 (2005): 95–97. http://dx.doi.org/10.1177/107602960501100112.

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20

Simms, H. Hank, and R. DʼAmico. "STUDIES ON POLYMORPHONUCLEAR LEUKOCYTE BACTERICIDAL FUNCTION." Shock 7, no. 2 (1997): 84–89. http://dx.doi.org/10.1097/00024382-199702000-00002.

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21

Simms, H. Hank, and R. DʼAmico. "STUDIES ON POLYMORPHONUCLEAR LEUKOCYTE BACTERICIDAL FUNCTION." Shock 7, no. 5 (1997): 339–44. http://dx.doi.org/10.1097/00024382-199705000-00005.

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22

Kaufmann, I., A. Hoelzl, T. Hummel, F. Schliephake, and M. Thiel. "POLYMORPHONUCLEAR LEUKOCYTE DYSFUNCTION SYNDROME IN SEPSIS." Shock 21, Supplement (2004): 14. http://dx.doi.org/10.1097/00024382-200403001-00055.

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23

Glette, Johan, Claus Ola Solberg, and Vidar Lehmann. "FACTORS INFLUENCING HUMAN POLYMORPHONUCLEAR LEUKOCYTE CHEMILUMINESCENCE." Acta Pathologica Microbiologica Scandinavica Series C: Immunology 90C, no. 1-6 (2009): 91–95. http://dx.doi.org/10.1111/j.1699-0463.1982.tb01423.x.

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24

Fumarulo, R., D. Giordano, A. Laforgia, A. Larocca, and M. Quarto. "Salivary effects on polymorphonuclear leukocyte functions." Oral Microbiology and Immunology 8, no. 2 (1993): 125–27. http://dx.doi.org/10.1111/j.1399-302x.1993.tb00558.x.

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25

Cavalot, F., G. Anfossi, I. Russo, et al. "Insulin Stimulates the Polymorphonuclear Leukocyte Chemokinesis." Hormone and Metabolic Research 25, no. 06 (1993): 321–22. http://dx.doi.org/10.1055/s-2007-1002109.

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26

PEASE, C. T., M. FENNELL, R. C. D. STAUGHTON, and D. A. BREWERTON. "Polymorphonuclear leukocyte function in psoriasis vulgaris." British Journal of Dermatology 117, no. 2 (1987): 161–67. http://dx.doi.org/10.1111/j.1365-2133.1987.tb04112.x.

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27

CHIARACASSONE, M. "Acute stress and polymorphonuclear leukocyte function." Pharmacological Research 26 (September 1992): 292. http://dx.doi.org/10.1016/1043-6618(92)91292-o.

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28

Khairy, Mahnouch, Dominique Lasne, Aymeric Amelot, et al. "Polymorphonuclear leukocyte and monocyte activation induced by plasma from patients with heparin-induced thrombocytopenia in whole blood." Thrombosis and Haemostasis 92, no. 12 (2004): 1411–19. http://dx.doi.org/10.1160/th03-10-0649.

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SummaryHeparin-induced thrombocytopenia (HIT), a severe complication of heparin therapy, results from platelet activation by heparin-dependent antibodies. Previously, we have shown that plasma from patients with HIT (HIT plasma) induces leukocyteplatelet aggregation in blood. In this report, we examined leukocyte activation by HIT plasma and the contribution of heparin and platelets to this activation, in whole blood. Degranulation of leukocytes from HIT patients was evaluated as a leukocyte activation marker. We showed that polymorphonuclear leukocytes (PMN) and monocytes were the leukocyte subpopulations involved in platelet-leukocyte aggregation induced by HIT plasma in healthy donor blood. PMN and monocyte activation, reflected by increased surface expression of the CD11b adhesion molecule, was induced by HIT plasma in a heparin-dependent manner. The CD11b increase induced by HIT plasma was observed on PMN only when they were associated with platelets. Moreover, the increased CD11b expression on monocytes and PMN correlated strongly with the degree of platelet adhesion to these cells. Degranulation of leukocytes from HIT patients and control subjects (non-HIT heparin-treated patients and healthy subjects) was evaluated in vivo by measuring the plasma myeloperoxidase concentration. HIT plasma contained higher myeloperoxidase concentrations than control plasma, suggesting leukocyte degranulation during HIT. In conclusion, this study provides the first evidence that PMN activation is induced by HIT plasma. HIT plasma induced PMN and monocyte activation in a heparin-dependent manner. In whole blood, platelet association with monocytes and PMN, and the activation of these leukocytes by HIT plasma were interrelated. Finally, leukocyte degranulation could be involved in HIT physiopathology.

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29

MELBY, KJETIL, TORE MIDTVEDT, and MIKLOS DEGRÉ. "EFFECT OF HUMAN LEUKOCYTE INTERFERON ON PHAGOCYTIC ACTIVITY OF POLYMORPHONUCLEAR LEUKOCYTES." Acta Pathologica Microbiologica Scandinavica Series B: Microbiology 90B, no. 1-6 (2009): 181–84. http://dx.doi.org/10.1111/j.1699-0463.1982.tb00102.x.

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30

Graham, John. "Isolation of Human Polymorphonuclear Leukocytes (Granulocytes) from a Leukocyte-Rich Fraction." Scientific World JOURNAL 2 (2002): 1393–96. http://dx.doi.org/10.1100/tsw.2002.831.

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Human peripheral blood polymorphonuclear leukocytes (PMNs) or granulocytes from a leukocyte-rich plasma (LRP) are banded at an interface between two layers of iodixanol. If the denser layer of iodixanol is omitted the PMNs may alternatively be pelleted. The procedure can be adapted to blood from other species by small changes to the density of the two iodixanol layers. The method works optimally with EDTA- or citrate-anticoagulated blood.

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31

Pearse, D. B., and J. T. Sylvester. "Spontaneous injury in isolated sheep lungs: role of resident polymorphonuclear leukocytes." Journal of Applied Physiology 72, no. 6 (1992): 2475–81. http://dx.doi.org/10.1152/jappl.1992.72.6.2475.

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Perfusion of isolated sheep lungs with homologous blood caused pulmonary hypertension and edema that was not altered by depletion of perfusate polymorphonuclear (PMN) leukocytes (D. B. Pearse et al., J. Appl. Physiol. 66: 1287–1296, 1989). The purpose of this study was to evaluate the role of resident PMN leukocytes in this injury. First, we quantified the content and activation of lung PMN leukocytes before and during perfusion of eight isolated sheep lungs with a constant flow (100 ml.kg-1.min-1) of homologous blood. From measurements of myeloperoxidase (MPO) activity, we estimated that the lungs contained 1.2 x 10(10) PMN leukocytes, which explained why the lung PMN leukocyte content, measured by MPO activity and histological techniques, did not increase significantly with perfusion, despite complete sequestration of 2.0 x 10(9) PMN leukocytes from the perfusate. MPO activities in perfusate and lymph supernatants did not increase during perfusion, suggesting that lung PMN leukocytes were not activated. Second, we perfused lungs from 6 mechlorethamine-treated and 6 hydroxyurea-treated sheep with homologous leukopenic blood and compared them with 11 normal lungs perfused similarly. Despite marked reductions in lung PMN leukocyte concentration, there were no differences in pulmonary arterial pressure, lymph flow, or reservoir weight between groups. Extravascular lung water was greater in both groups of leukopenic lungs. These results suggest that resident PMN leukocytes did not contribute to lung injury in this model.

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32

Ulgen S Yaramis, CP, E. Rayaman, U. Soyogul Gurer, ME Or, and AO Sehirli. "Effects of inactivated Parapoxvirus ovis on polymorphonuclear leukocyte function and myeloperoxidase activity in horses." Veterinární Medicína 59, No. 12 (2014): 631–36. http://dx.doi.org/10.17221/7823-vetmed.

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Immunomodulatory products have been used for years in veterinary medicine. Inactivated Parapoxvirus ovis (iPPVO) is currently used in equine medicine as an immunomodulator to improve the immune system and as a prophylactic treatment to prevent or treat infectious diseases. This study was designed to determine the effects of iPPVO on polymorphonuclear leukocyte (PMNL) function (phagocytosis and intracellular killing activity) and the myeloperoxidase (MPO) activity of PMNLs in horses. Twenty-four healthy English thoroughbred horses with an average age of 11 years were included in the study. Venous blood samples (10 ml) were taken before (agent-free controls) and after the administration of iPPVO (2 ml i.m. injection on Days 1, 3, and 5). PMNLs (1&nbsp;&times;&nbsp;10<sup>7</sup> cells/ml) were isolated from venous blood containing EDTA (0.1 g/ml) with Ficoll-Hypaque gradient centrifugation. Cellular phagocytosis and intracellular killing activities were assayed using a modification of Alexander&rsquo;s method before and after treatment with iPPVO. MPO activity was also measured. The administration of iPPVO significantly increased the phagocytic, intracellular killing, and MPO activities of equine PMNLs (P = 0.0058, P&nbsp;= 0.0050, and P = 0.0070, respectively). This study demonstrates a strong correlation between MPO activity and PMNL function. The administration of iPPVO to horses has a supportive effect on their cellular immunity and an immunomodulatory effect against equine viral infections.

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33

Kirchhofer, Daniel, Markus A. Riederer, and Hans R. Baumgartner. "Specific Accumulation of Circulating Monocytes and Polymorphonuclear Leukocytes on Platelet Thrombi in a Vascular Injury Model." Blood 89, no. 4 (1997): 1270–78. http://dx.doi.org/10.1182/blood.v89.4.1270.

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AbstractThe adhesion of leukocytes to platelets deposited at the site of vascular injury may represent an important mechanism by which leukocytes contribute to hemostasis and thrombosis. In this study, we examined whether, in comparison with their distribution in circulating blood, certain leukocyte types are enriched at sites of platelet deposition. We used an experimental vascular injury model, in which human fibrillar collagen was exposed to anticoagulated human whole blood flowing through parallel-plate chambers (venous shear rate, 65/s). The platelet-adherent leukocytes were detached by EDTA treatment and analyzed by flow cytometry using cell-type–specific antibodies. The predominant leukocytes found in platelet thrombi were polymorphonuclear leukocytes, accounting for 76% of bound leukocytes (62% in circulating blood), whereas T and B lymphocytes did not significantly accumulate on thrombi, comprising a fraction of less than 5% (32% in circulating blood). Monocytes constituted 16% of platelet thrombus-bound leukocytes, which represents an almost fourfold enrichment as compared with their proportion in circulating blood. Almost identical results were obtained when we analyzed leukocytes adhering to platelet monolayers, which were formed by blocking glycoprotein IIb-IIIa, thus preventing platelet aggregation on top of the collagen-adherent platelets. Furthermore, leukocyte adhesion to platelet monolayers was completely inhibited by an anti-P-selectin antibody (50% inhibitory concentration, 0.3 μg/mL), whereas it reached a plateau at about 70% inhibition on platelet thrombi. This difference could be explained by a possible function of glycoprotein IIb-IIIa in leukocyte immobilization to thrombi or by the high local concentration of P-selectin in the growing thrombi. The results suggest that, because of their known abilities to promote coagulation and thrombolysis, the monocytes and polymorphonuclear leukocytes accumulating on forming platelet thrombi could play an important role in modulating thrombotic and hemostatic processes.

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34

Hopps, Eugenia, Rosalia Lo Presti, and Gregorio Caimi. "Pathophysiology of polymorphonuclear leukocyte in arterial hypertension." Clinical Hemorheology and Microcirculation 41, no. 3 (2009): 209–18. http://dx.doi.org/10.3233/ch-2009-1173.

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35

Nose, T., Y. Segawa, M. Nozaki, K. Tsurumi, and H. Fujimura. "Polymorphonuclear leukocyte responses in adjuvant arthritis rats." European Journal of Pharmacology 183, no. 6 (1990): 2247. http://dx.doi.org/10.1016/0014-2999(90)93785-o.

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36

Usami, S., S. L. Wung, B. A. Skierczynski, R. Skalak, and S. Chien. "Locomotion forces generated by a polymorphonuclear leukocyte." Biophysical Journal 63, no. 6 (1992): 1663–66. http://dx.doi.org/10.1016/s0006-3495(92)81745-9.

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37

de Gaetano, Giovanni, Chiara Cerletti, and Virgilio Evangelista. "Recent Advances in Platelet-Polymorphonuclear Leukocyte Interaction." Pathophysiology of Haemostasis and Thrombosis 29, no. 1 (1999): 41–49. http://dx.doi.org/10.1159/000022459.

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38

Vila, N., M. Elena, R. Deulofeu, and A. Chamorro. "Polymorphonuclear leukocyte elastase in patients with stroke." Acta Neurologica Scandinavica 100, no. 6 (2009): 391–94. http://dx.doi.org/10.1111/j.1600-0404.1999.tb01058.x.

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39

Topham, Matthew K., Holly J. Carveth, Thomas M. McIntyre, Stephen M. Prescott, and Guy A. Zimmerman. "Human endothelial cells regulate polymorphonuclear leukocyte degranulation." FASEB Journal 12, no. 9 (1998): 733–46. http://dx.doi.org/10.1096/fasebj.12.9.733.

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40

Antony, V. B., C. L. Owen, and D. English. "Polymorphonuclear leukocyte cytoplasts mediate acute lung injury." Journal of Applied Physiology 65, no. 2 (1988): 706–13. http://dx.doi.org/10.1152/jappl.1988.65.2.706.

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Injection of phorbol 12-myristate 13-acetate (PMA) into polymorphonuclear leukocyte (PMN)-depleted, PMN cytoplast-repleted New Zealand White rabbits caused the development of acute lung injury in vivo. PMN cytoplasts are nucleus- and granule-free vesicles of cytoplasm capable of releasing toxic O2 radicals but incapable of releasing granule enzymes. PMN cytoplasts when activated by PMA reduced 66 +/- 12.7 nmol of cytochrome c compared with 2.6 +/- 0.7 nmol in their resting state and did not release a significant quantity of granule enzymes (P greater than 0.05). Injection of PMA into New Zealand White rabbits caused a significant decrease (P less than 0.05) in the number of circulating cytoplasts. Increases in lung weight-to-body weight ratios in PMA-treated rabbits (9.8 +/- 0.5 X 10(-3] compared with saline-treated rabbits (5.3 +/- 0.2 X 10(-3] were also noted. Levels of angiotensin-converting enzyme in lung lavage as well as the change in alveolar-arterial O2 ratio correlated with the numbers of cytoplasts in lung lavage (P = 0.001, r = 0.84 and P = 0.0166, r = 0.73, respectively). Albumin in lung lavage increased to 1,700 +/- 186 mg/ml in PMA-treated rabbits from 60 +/- 30 mg/ml in saline-treated rabbits. These changes were attenuated by pretreatment of rabbits with dimethylthiourea (DMTU). In vitro, cytoplasts were able to mediate increases in endothelial monolayer permeability. This was evidenced by increases in fractional transit of albumin across endothelial monolayers when treated with PMA-activated cytoplasts (0.08 +/- 0.01 to 0.28 +/- 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

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41

Kuratsuji, Tadatoshi, Shunichi Shimizu, Kunihisa Takagi, Hideji Hanabusa, Mitsuru Osano, and Yasuo Ichihashi. "Effects of Pentoxifylline on Polymorphonuclear Leukocyte Function." Pediatrics International 27, no. 4 (1985): 547–51. http://dx.doi.org/10.1111/j.1442-200x.1985.tb00678.x.

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42

Krause, PJ, HL Malech, J. Kristie, et al. "Polymorphonuclear leukocyte heterogeneity in neonates and adults." Blood 68, no. 1 (1986): 200–204. http://dx.doi.org/10.1182/blood.v68.1.200.200.

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Abstract We have used a mouse monoclonal antibody (31D8) to determine whether differences in neutrophil (PMN) subpopulations might help explain decreased PMN chemotaxis in neonates compared with that of adults. 31D8 has been shown to bind heterogeneously to adult PMNs. Approximately 80% of the PMNs that strongly bind 31D8 (31D8 “bright”) are the same cells that depolarize and migrate chemotactically when stimulated with the chemoattractant N-formyl-methionylleucylphenylalanine, while the 20% that weakly bind 31D8 fail to similarly respond. All neonatal PMNs bound 31D8 heterogeneously. There was a smaller population of 31D8 “bright” cells in neonates at birth (76% +/- 6%, n = 45) compared with that of neonates at three to 15 days of age (82% +/- 5%, n = 10, P less than 0.002) and both were smaller than that of adults (88% +/- 4%, n = 45, P less than 0.001 and P less than 0.001). Neonatal cord PMNs, which traversed a micropore filter in a modified Boyden chemotaxis chamber in the presence of a chemoattractant, had an increased percentage of 31D8 “bright” cells (89% +/- 7%) than did PMNs which remained above the filter (82% +/- 7%, n = 10, P = 0.034). PMN chemotaxis was less in neonates at birth (32.7 +/- 4.5 micron) than at three to six days of age (36.8 +/- 11.3 micron) and both were decreased compared with that of adults (69.1 +/- 12.4 micron, P less than 0.001 and P less than 0.001). These findings indicate that decreased PMN chemotaxis in neonates may be due in part to a smaller PMN subpopulation of highly motile cells.

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43

Krause, PJ, HL Malech, J. Kristie, et al. "Polymorphonuclear leukocyte heterogeneity in neonates and adults." Blood 68, no. 1 (1986): 200–204. http://dx.doi.org/10.1182/blood.v68.1.200.bloodjournal681200.

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Abstract:

We have used a mouse monoclonal antibody (31D8) to determine whether differences in neutrophil (PMN) subpopulations might help explain decreased PMN chemotaxis in neonates compared with that of adults. 31D8 has been shown to bind heterogeneously to adult PMNs. Approximately 80% of the PMNs that strongly bind 31D8 (31D8 “bright”) are the same cells that depolarize and migrate chemotactically when stimulated with the chemoattractant N-formyl-methionylleucylphenylalanine, while the 20% that weakly bind 31D8 fail to similarly respond. All neonatal PMNs bound 31D8 heterogeneously. There was a smaller population of 31D8 “bright” cells in neonates at birth (76% +/- 6%, n = 45) compared with that of neonates at three to 15 days of age (82% +/- 5%, n = 10, P less than 0.002) and both were smaller than that of adults (88% +/- 4%, n = 45, P less than 0.001 and P less than 0.001). Neonatal cord PMNs, which traversed a micropore filter in a modified Boyden chemotaxis chamber in the presence of a chemoattractant, had an increased percentage of 31D8 “bright” cells (89% +/- 7%) than did PMNs which remained above the filter (82% +/- 7%, n = 10, P = 0.034). PMN chemotaxis was less in neonates at birth (32.7 +/- 4.5 micron) than at three to six days of age (36.8 +/- 11.3 micron) and both were decreased compared with that of adults (69.1 +/- 12.4 micron, P less than 0.001 and P less than 0.001). These findings indicate that decreased PMN chemotaxis in neonates may be due in part to a smaller PMN subpopulation of highly motile cells.

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44

Rollins, T. E., and M. S. Springer. "Identification of the polymorphonuclear leukocyte C5a receptor." Journal of Biological Chemistry 260, no. 12 (1985): 7157–60. http://dx.doi.org/10.1016/s0021-9258(17)39585-6.

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Caimi, G. "Polymorphonuclear leukocyte integrin profile in essential hypertension." American Journal of Hypertension 13, no. 9 (2000): 1051–52. http://dx.doi.org/10.1016/s0895-7061(00)01189-4.

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Sakata, Miki, Robert A. Sack, Sonal Sathe, Brien Holden, and Ann R. Beaton. "Polymorphonuclear leukocyte cells and elastase in tears." Current Eye Research 16, no. 8 (1997): 810–19. http://dx.doi.org/10.1076/ceyr.16.8.810.8992.

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Chusid, M. J., and S. D. Davis. "Polymorphonuclear Leukocyte Kinetics in Experimentally Induced Keratitis." Archives of Ophthalmology 103, no. 2 (1985): 270–74. http://dx.doi.org/10.1001/archopht.1985.01050020122034.

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De Gottardi, Andrea. "Polymorphonuclear Leukocyte Count in Spontaneous Bacterial Peritonitis." JAMA 300, no. 3 (2008): 282. http://dx.doi.org/10.1001/jama.2008.28.

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Borregaard, Niels, and Jack B. Cowland. "Granules of the Human Neutrophilic Polymorphonuclear Leukocyte." Blood 89, no. 10 (1997): 3503–21. http://dx.doi.org/10.1182/blood.v89.10.3503.

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Borregaard, Niels, and Jack B. Cowland. "Granules of the Human Neutrophilic Polymorphonuclear Leukocyte." Blood 89, no. 10 (1997): 3503–21. http://dx.doi.org/10.1182/blood.v89.10.3503.3503_3503_3521.

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