Alteration of Polymorphonuclear Neutrophil Surface Receptor Expression and Migratory Activity After Isolation: Comparison of Whole Blood and Isolated PMN Preparations from Normal and Postfracture Trauma Patients

Heat-killed (HK) Mycobacterium obuense is a novel immunomodulator, currently undergoing clinical evaluation as an immunotherapeutic agent in the treatment of cancer. Here, we examined the effect of in vitro exposure to HK M. obuense on the expression of different categories of surface receptors on human blood myeloid (m) and plasmacytoid (p) DCs. Moreover, we have characterized the cytokine and chemokine secretion patterns of purified total blood DCs stimulated with HK M. obuense. HK M. obuense significantly up-regulated the expression of CD11c, CD80, CD83, CD86, CD274 and MHC class II in whole-blood mDCs and CD80, CD123 and MHC class II in whole-blood pDCs. Down-regulation of CD195 expression in both DC subpopulations was also noted. Further analysis showed that HK M. obuense up-regulated the expression of CD80, CD83 and MHC class II on purified blood DC subpopulations. TLR2 and TLR1 were also identified to be engaged in mediating the HK M. obuense-induced up-regulation of surface receptor expression on whole blood mDCs. In addition, our data demonstrated that HK M. obuense augmented the secretion of CCL4, CCL5, CCL22, CXCL8, IL-6, IL-12p40 and TNF-α by purified total blood DCs. Taken together, our data suggest that HK M. obuense exerts potent differential immunomodulatory effects on human DC subpopulations.

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Matrix protein regulation of PMN oxidative metabolism during ischemia

AJP Cell Physiology ◽

10.1152/ajpcell.1994.266.3.c637 ◽

1994 ◽

Vol 266 (3) ◽

pp. C637-C647 ◽

Cited By ~ 30

Author(s):

H. Simms ◽

R. D'Amica

Keyword(s):

Oxidative Metabolism ◽

Superoxide Anion ◽

Matrix Protein ◽

Receptor Expression ◽

Matrix Proteins ◽

Polymorphonuclear Neutrophil ◽

Acute Ischemia ◽

H2o2 Production ◽

Superoxide Anion Production ◽

Surface Receptor

Matrix proteins upregulate polymorphonuclear neutrophil (PMN) oxidative metabolism in a normoxic environment. We sought to investigate the relationship between matrix proteins and adherent PMN oxidative metabolism during acute ischemia. PMN adherent to buffer, fibronectin, Arg-Gly-Asp-Ser (RGDS), or laminin were placed in either normoxic or ischemic media. PMN adherence, superoxide anion production, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) formazan production, and surface receptor expression (CD64, CD32w, CD16, CD35, and CD11b/CD18) using monoclonal antibodies directed against these receptors were assayed. Ischemia increased PMN adherence unless the PMN were adhered to fibronectin or RGDS. Ischemia reduced PMN superoxide anion, MTT formazan, and H2O2 production unless the PMN were adhered to fibronectin or RGDS. Fibronectin and RGDS prevented ischemic-induced suppression of FcR expression. Immunofluorescent studies demonstrated capping and clustering of PMN Fc and complement receptors during ischemia while adhered on matrix proteins. These results demonstrate that 1) ischemia suppresses matrix protein upregulation of PMN oxidative metabolism, which is restored by fibronectin; 2) fibronectin-mediated restoration of PMN oxidative metabolism involves the binding epitope of fibronectin; and 3) fibronectin maintains PMN oxidative metabolism during ischemia in part by maintaining PMN FcR on the cell surface and by recruiting a new population of PMN capable of undergoing oxidative metabolism.

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Activation State of the Circulating Neutrophil in Isolated Chest Trauma Patients: Characterization of Surface Receptor Expression

Journal of Trauma & Treatment ◽

10.4172/2167-1222.1000363 ◽

2017 ◽

Vol 06 (01) ◽

Cited By ~ 1

Author(s):

Eman Nasreldin ◽

Mahmoud Khairy

Keyword(s):

Chest Trauma ◽

Receptor Expression ◽

Trauma Patients ◽

Surface Receptor

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Changes in neutrophil surface receptor expression, degranulation, and respiratory burst activity after moderate- and high-intensity exercise

Journal of Applied Physiology ◽

10.1152/japplphysiol.01331.2003 ◽

2004 ◽

Vol 97 (2) ◽

pp. 612-618 ◽

Cited By ~ 54

Author(s):

Jonathan Peake ◽

Gary Wilson ◽

Matthew Hordern ◽

Katsuhiko Suzuki ◽

Kanemitsu Yamaya ◽

...

Keyword(s):

Respiratory Burst ◽

High Intensity ◽

Burst Activity ◽

Receptor Expression ◽

Intense Exercise ◽

Respiratory Burst Activity ◽

Cd16 Expression ◽

Neutrophil Degranulation ◽

Surface Receptor ◽

Neutrophil Surface

Intense exercise stimulates the systemic release of a variety of factors that alter neutrophil surface receptor expression and functional activity. These alterations may influence resistance to infection after intense exercise. The aim of this study was to examine the influence of exercise intensity on neutrophil receptor expression, degranulation (measured by plasma and intracellular myeloperoxidase concentrations), and respiratory burst activity. Ten well-trained male runners ran on a treadmill for 60 min at 60% [moderate-intensity exercise (MI)] and 85% maximal oxygen consumption [high-intensity exercise (HI)]. Blood was drawn immediately before and after exercise and at 1 h postexercise. Immediately after HI, the expression of the neutrophil receptor CD16 was significantly below preexercise values ( P < 0.01), whereas MI significantly reduced CD35 expression below preexercise values ( P < 0.05). One hour after exercise at both intensities, there was a significant decline in CD11b expression ( P < 0.05) and a further decrease in CD16 expression compared with preexercise values ( P < 0.01). CD16 expression was lower 1 h after HI than 1 h after MI ( P < 0.01). Immediately after HI, intracellular myeloperoxidase concentration was less than preexercise values ( P < 0.01), whereas plasma myeloperoxidase concentration was greater ( P < 0.01), indicating that HI stimulated neutrophil degranulation. Plasma myeloperoxidase concentration was higher immediately after HI than after MI ( P < 0.01). Neutrophil respiratory burst activity increased after HI ( P < 0.01). In summary, both MI and HI reduced neutrophil surface receptor expression. Although CD16 expression was reduced to a greater extent after HI, this reduction did not impair neutrophil degranulation and respiratory burst activity.

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