Search results

1

Effect of IL-18 on IL-lbeta and sIL-1RII production by human neutrophils

100%

Jablonska E., Izycka A., Wawrusiewicz N.

Archivum Immunologiae et Therapiae Experimentalis

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2002

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vol. 50

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issue 2

139-142

EN

In the present study we investigated the effect of interleukin-18 (IL-18) on the production of interleukin-1beta (IL-1beta) and soluble interleukin-1 receptor II (sIL-lRII) by human neutrophils. The results obtained indicate that recombinant human interleukin-18 (rhIL-18) induces IL-l beta and, to a lesser extent, sIL-1RII production by human neutrophil isolated from peripheral blood. However, this effect was less important than lipopolysaccharide (LPS) stimulation. Additionally, our observations suggest that IL-18 can induce priming of neutrophils for IL-l beta and, to a lesser extent, sIL-lRII production by LPS--stimulated cells. The ability of IL-18 to serve as an effective modulator for IL-l betaand its regulatory protein may have significance in the inflammatory and immune reactions mediated by IL-l beta.

2

Neutrophile activation by bacterial endotoxins

100%

Klink M., Kaca W.

Postępy Higieny i Medycyny Doświadczalnej

|

1996

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vol. 50

|

issue 4

333-350

EN

The endotoxin (lipopolysaccharide, LPS), major component of Gram-negative bacteria cell wall, activate numerous types of cells, neutrophile included. The chemical compositions of polysaccharide (O-specific polysaccharide and core oligosaccharide) and hydrophobic lipid A parts of LPS are presented. The bindings of LPSs to neutrophiles resulted in signal transduction and neutrophiles activation. Neutrophiles, under LPS stimulation, generate oxygen radicals, nitric oxide and other components of inflammatory processes.

3

New biodefense strategies by neutrophils

80%

Ishikawa F., Miyazaki S.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 3

226-233

EN

Chemokines and other chemotactic factors induce neutrophils, macrophages, and dendritic cells to migrate to an inflammatory site and efficiently ingest and destroy infective microorganisms. Moreover, antigen-presenting cells, such as macrophages and dendritic cells, present the microbial antigens via major histocompatibility complex class II molecules, resulting in the activation of specific CD4 T cells. Since neutrophils have a short life-span and are highly susceptible to apoptosis, their role in antigen presentation has been questioned. However, various pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6, tumor necrosis factor a, and interferon g, produced at the site of inflammation activate neutrophils and suppress apoptotic death. These cytokine-activated neutrophils show enhanced expression of cell surface molecules and become as competent as dendritic cells and macrophages in their ability of antigen presentation. Traditionally, neutrophils are known to be responsible for innate immunity, and recently they are also considered to be intimately associated with the establishment of acquired immunity. In the present review on the role of neutrophils we describe both classic innate and acquired immunity.

4

Reactive oxygen intermediates and serum antioxidative system in patients with chronic C hepatitis treated with IFN-alpha and thymus factor X

80%

Jablonowska E., Tchorzewski H., Lewkowicz P., Kuydowicz J.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 6

529-533

EN

In this study, the chemiluminescence (CL) of peripheral blood polymorphonuclear leukocytes (PMNLs) and the serum total antioxidative system (TAS) were assessed in patients with chronic C hepatitis (CCH) before and after 3 and 6 months of treatment with interferon (IFN)- and thymus factor X (TFX). The study included 26 patients with CCH aged between 25?63 years (mean: 42.67). Combined therapy with IFN-alpha 2a and a TFX preparation was applied. PMNL metabolic activity was assessed applying the whole-blood CL method. We measured CL response of neutrophils unstimulated and stimulated by opsonized zymosan, N-formyl-methionyl-leucyl-phenylalanine (N-fMLP), and phorbol-myristate-acetate (PMA) without and after priming with tumor necrosis factor alpha (10 ng/ml). The assessment of serum TAS was performed directly before the beginning of therapy with IFN-alpha and TFX and after 3 and 6 months of the treatment. A colorimetric method based on the reduction of the cationic radical ABTS+ (cation 2, 2'-azido-bis-[3-ethylobenzothiazolino-6-sulfonate]) in the presence of serum antioxidants was used. As a result of the treatment with IFN-alpha and TFX, the formation of free oxygen radicals by resting (unprimed) neutrophils increased statistically significantly both without stimulation and following stimulation by fMLP and PMA. A statistically significant increase in the serum antioxidant capacity was observed, which suggests the induction of compensatory processes. Increased in vitro reactive oxygen species production by both stimulated and unstimulated peripheral blood neutrophils of patients with CCH was observed. Treatment with IFN-alpha and TFX resulted in a compensatory increase in serum antioxidative capacity.

5

TNF-alpha priming effect on polymorphonuclear leukocyte reactive oxygen species generation and adhesion molecule expression in hemodialyzed patients

80%

Rysz J., Banach M., Stolarek R. A., Pasnik J., Cia?kowska-Rysz A., Markuszewski L., Baj Z.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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vol. 54

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issue 3

209-215

EN

Introduction: The study aimed to assess reactive oxygen species generation and the expressions of some surface antigens on polymorphonuclear leukocytes (PMNs) in patients on regular hemodialysis (HD) treatment. Materials and Methods: The respiratory burst of PMNs was determined with luminol-dependent chemiluminescence (CL) in resting cells and following N-formyl-methionyl-leucyl-phenylalanine (fMLP), phorbol 12-myristate 13-acetate (PMA), or opsonized zymosan (OZ) stimulation and expressed in arbitrary CL units times assay-time (aUmin). The expressions of CD11b/CD18, CD10, and CD13 receptors were determined with flow cytometry. Results: Basal PMN CL was increased in HD patients to up to 1285129 aUmin compared with 89588 aUmin in healthy controls (p<0.05). The CL of unprimed PMNs increased after fMLP stimulation from 3085746 to 4529808 aUmin, and after OZ stimulation from 129451296 to 146781355 aUmin. PMA-stimulated CL of PMNs was similar to control values. The oxidative burst in PMNs from HD patients and healthy controls was similar in response to TNF-alpha alone. The CL of TNF- alpha-primed PMNs in HD patients was significantly lower than CL measured in healthy controls (p<0.05). The expressions of CD10 and CD13 metalloproteinase receptors were also increased (p<0.05). Although CD11b expression was significantly increased at rest and after fMLP stimulation, the expression of another beta-integrin heterodimer compound, CD18, was not increased. Conclusions: These results provide evidence that TNF- priming of PMNs is down-regulated in HD patients despite constitutive up-regulation of resting cytotoxicity and enhanced expression of adhesion and metalloproteinase receptors.

6

Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

80%

Kobayashi S. D., DeLeo F. R.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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vol. 51

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issue 1

1-8

EN

Polymorphonuclear leukocytes (PMNs or neutrophils) are essential components of the innate immune system in humans and function primarily to eliminate invading microorganisms. Neutrophil influx to sites of infection is desirable because it also initiates an inflammatory response. Paradoxically, PMNs are also intimately associated with inflammatory disease. As part of normal neutrophil turnover in humans and to limit inflammatory potential, PMNs undergo programmed cell death or apoptosis. Several host factors, including cytokines and growth factors, are capable of extending neutrophil survival, and thus capacity to fight infection. On the other hand, phagocytosis of bacterial pathogens generally accelerates PMN apoptosis. Due in part to the extensive complexity of programmed cell death, relatively little is known about signaling pathways that govern these processes in PMNs. Recently, microarray strategies have been employed to gain an understanding of these processes in activated PMNs, and new evidence indicates that gene transcription is important in the regulation of neutrophil apoptosis and thus inflammation. A series of provocative discoveries led to the hypothesis that neutrophil programmed cell death is the result of an apoptosis differentiation program, a final stage of transcriptionally regulated PMN maturation or hematopoietic differentiation. Further characterization of the apoptosis differentiation program and associated biochemical pathways in mature PMNs will likely yield important insights into the resolution of inflammation and infection.

7

Regulation of the NADPH oxidase activity and anti-microbial function of neutrophils by arachidonic acid

80%

Hii C. S., Ferrante A.

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2007

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vol. 55

|

issue 2

99-110

EN

Arachidonic acid (AA), a second-messenger molecule released from membrane phospholipids by phospholipase A2 in activated cells, is a stimulator of neutrophil responses, including the oxygen-dependent respiratory burst. The polyunsaturated fatty acid is also the precursor of biologically active eicosanoids. There are several mechanisms by which AA stimulates the respiratory burst. These include the direct binding of AA to S100 proteins which regulate the assembly of the NADPH oxidase as well as the activation of key signaling molecules which control the respiratory burst. Arachidonic acid also stimulates it own release from membrane phospholipids and this contributes to optimal respiratory burst activity. Thus, increased levels of AA at sites of inflammation will influence the magnitude and course of the inflammatory response, not only by directly affecting the function of infiltrating neutrophils and other leukocytes, but also through its metabolites generated by lipoxygenases and cyclooxygenases.

8

Phagocyte NADPH oxidase: a multicomponent enzyme essential for host defenses

80%

El-Benna J., Dang P. M.-C., Gougerot-Pocidalo A.-M., Elbim C.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 3

199-206

EN

Phagocytes such as neutrophils and monocytes play an essential role in host defenses against microbial pathogens. Reactive oxygen species (ROS), such as superoxide anion, hydrogen peroxide, the hydroxyl radical, and hypochlorous acid, together with microbicidal peptides and proteases, constitute their antimicrobial arsenal. The enzyme responsible for superoxide anion production and, consequently, ROS generation, is called NADPH oxidase or respiratory burst oxidase. This multicomponent enzyme system is composed of cytosolic proteins (p47phox, p67phox, p40phox, and rac1/2) and membrane proteins (p22phox and gp91phox, which form cytochrome b558) which assemble at membrane sites upon cell activation. The importance of this enzyme in host defenses is illustrated by a life-threatening genetic disorder called chronic granulomatous disease in which the phagocyte enzyme is dysfunctional, leading to life-threatening bacterial and fungal infections. Also, because ROS can damage surrounding tissues, their production, and thus NADPH oxidase activation, must be tightly regulated. This review describes the structure and activation of the neutrophil NADPH enzyme complex.

9

Effect of cardiopulmonary bypass on neutrophil activity in pediatric open-heart surgery

80%

Pasnik J., Siniewicz K., Moll J., Moll J. A., Baj Z., Sysa A., Zeman K.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 3

272-277

EN

The nature of the participation of neutrophils in the post-cardiopulmonary bypass (CPB) inflammatory response is not very clear. The aim of our study was to investigate alterations in neutrophil phagocytic activity and adhesion molecule expression on these cells in children during and after CPB. Twenty-one children aged 6?33 months with congenital heart disease, scheduled for primary corrective surgery, were enrolled. The expressions of CD11b adhesion molecules and Fcg receptor on neutrophils and their phagocytic activity were evaluated. The studied markers were sequentially measured before, at the initiation of, and after CPB. During the course of the operation, CD11b molecule expression on neutrophils showed a slight elevation at the start of CPB (876.5104.8 mean fluorescence intensity, MFI, vs. 768.1178.2; p=0.0047), followed by a significant decrease to 689.01166.7 MFI after completion of the procedure. The expression of CD11b molecule on neutrophils measured at the end of CPB inversely correlated with the duration of CPB (r= ?0.68, p=0.00059). The expression of CD16 antigen dropped significantly at the start of CPB (1164.6307.3 MFI vs. 1327.4345.3 MFI; p=0.0007) and remained decreased until the end of CPB (814.0198.1 MFI). These findings suggest that the characteristics of the neutrophil response to cardiac surgery appear to depend on many factors. We demonstrated a link between the duration of CPB and adhesion molecule expression on neutrophils.

10

Neutrophil recognition of bacterial DNA and Toll-like receptor 9-dependent and independent regulation of neutrophil function

80%

El_ K. D., Jozsef L., Filep J. G.

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issue 1

41-53

EN

Neutrophils are essential for host defense and detect the presence of invading microorganisms through recognition of pathogen-associated molecular patterns. Among these receptors are Toll-like receptors (TLRs). Neutrophils express all known TLRs except for TLR3. TLR9, localized intracellularly, is to date the best characterized sensor for bacterial DNA, containing short sequences of unmethylated CpG motifs, though TLR9-independent intracellular DNA recognition mechanism(s) may also exist. Bacterial DNA has profound impact on neutrophil functions; it promotes neutrophil trafficking in vivo, induces chemokine expression, regulates expression of adhesion molecules, enhances phagocyte activity, and rescues neutrophils from constitutive apoptosis. TLR9 stimulation results in alterations in cellular redox balance, peroxynitrite formation, activation of the mitogen-activated protein kinase, PI3-kinase, and Jun N-terminal kinase pathways and/or nuclear factor ?B and AP-1. These features identify an important role for bacterial DNA and TLR9 signaling in the regulation of neutrophil functions that are critical for optimal expression as well as for resolution of the inflammatory response.

11

Granules of human neutrophils

80%

Wysocka J., Lipartowska R., Lipska A.

Postępy Higieny i Medycyny Doświadczalnej

|

2001

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vol. 55

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issue 1

177-188

EN

The exocytosis of cytoplasmic granules plays a most important role in the regulation of many neutrophils functions: adhesion, phagocytosis, killing of bacteria and interaction with endothelial cells. Neutrophils contain following types of granules: azurophilic (primary) granules, specific (secondary) granules, gelatinase-rich tertiary granules and secretory vesicles. Neutrophil granules may be classified on the basis of their size, morphology, density or with reference to a given protein.

12

Circadian variations of histamine binding to lymphocytes and neutrophils and skin reactivity to histamine in atopic and healthy subjects

80%

Zak-Nejmark T., Nowak I. A., Kraus-Filarska M.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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vol. 54

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issue 4

283-287

EN

Intruction: Numerous pathophysiological conditions change during 24-hour periods. Histamine, the main mediator in allergic reactions, exerts a multiplicity of pathophysiological actions through binding to specific receptors on effector cells. Nocturnal exacerbation of symptoms occurs in many atopic diseases in which histamine is an important mediator. Nocturnal wheezing is a very common symptom of asthma. The aim of this study was to determine whether the binding of (fluorescein-labeled) histamine to cells participating in allergic-inflammatory processes (lymphocytes, neutrophils) and skin reactivity to histamine undergo circadian changes and to compare these phenomena in atopic asthmatic and healthy subjects. Materials and Methods: Blood samples were collected at 8 am, 2 pm, 8 pm, 2 am, and 8 am the next day. Histamine skin-prick tests were performed at the same times. Results: It was found that skin reactivity to histamine (wheal, erythema) in healthy subjects underwent significant circadian changes with acrophase at 8 am (wheal) or 8 pm (erythema), the lowest values being at night (2 am, p=0.017), in contrast to atopics, in whom the highest reactivity was found at night (2 am, p=0.002). Significant differences in the binding of fluorescein-labeled histamine between day (8 am?2 pm) and night (2 am) were observed for lymphocytes (p=0.006) and neutrophils (p=0.018). Conclusions: In the asthmatic group these changes were not significant. Circadian changes in both the binding of histamine by effector cells and skin reactivity to histamine were different in healthy and asthmatic subjects, and this may play a role in the pathomechanism, course, and chronopharmacotherapy of atopic diseases.

13

Proinflammatory cytokine inhibitors, TNF- and oxidative burst of polymorphonuclear leukocytes in the pathogenesis of sepsis in newborns

80%

Sikora J. P., Chlebna-Sokol D., Dabrowska I., Lipczynski D., Chrul S.

Archivum Immunologiae et Therapiae Experimentalis

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2001

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vol. 49

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issue 2

155-162

EN

This study was to evaluate the levels of the proinflammatory cytokine tumor necrosis factor alpha (TNF-) and the cytokine inhibitors soluble TNF- receptor (sTNFR) and IL-1 receptor antagonist (IL-1 ra) as well as the intensity of oxidative metabolism of peripheral blood polymorphonuclear leukocytes in the course of sepsis in newborns. An increase of TNF-, sTNFR and IL-1 ra concentrations was found in the blood serum of the patients at the time of diagnosis. This was further accompanied by polymorphonuclear leukocyte stimulation and, as a consequence of prolonged bacterial antigen stimulation, functional exhaustion of these cells and their diminished oxidative metabolism was observed. Within the same time period, an enhanced expression of p55 and p75 TNF- receptors on polymorphonuclear leukocyte cell surfaces was found. It was indicated that the applied pharmacotherapy caused a decrease of the initially elevated concentrations of TNF- and proinflammatory cytokine inhibitors (sTNFR, IL-1 ra). The intensive therapy of sepsis was associated with the increased oxidative burst of polymorphonuclear leukocytes along with the decrease of p55 and p75 expression on their cell surfaces.

14

iNOS expression and NO production by neutrophils in cancer patients

71%

Jablonska E., Puzewska W., Marcinczyk M., Grabowska Z.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 2

175-179

EN

The tumor-polymorphonuclear neutrophil (PMN) relationship can be altered by the release of toxic molecules, such as nitric oxide (NO). The aim of the present study was to examine the expression of the inducible synthase of NO (iNOS) and NO production by human neutrophils of patients with oral cavity cancer. For comparison we performed similar examinations in autologous peripheral blood mononuclear cells (PBMCs). PMNs and PBMCs were isolated from the whole blood of 27 patients with squamous cell carcinoma of the oral cavity. iNOS protein expression in these cells was detected by Western blot. Total nitrite as an indicator of NO concentrations in the culture supernatants and the serum of patients was measured using a colorimetric assay. The PMNs of oral cavity cancer patients showed a significantly lower intensity of iNOS expression than those of healthy controls. The PBMCs of patients showed a more intensive expression of iNOS than the PMNs, but a lower intensity than the PBMCs of the controls. The expression of iNOS in rhIL-6 and rhIL-15-stimulated PMNs and PBMCs of patients increased in comparison with unstimulated cells. We observed lower productions of NO by PMNs and PBMCs of patients than those of the control group. The results revealed that altered iNOS expression and NO production are more characteristic of PMNs than of PBMCs of patients with oral cavity cancer. Additionally, this study provided new information about IL-6 and IL-15 activity in a tumor-bearing host.

15

Temperature can prime human peripheral blood neutrophils in a p38MAPKa-dependent manner

71%

Jozefowicz-Okonkwo G., Nowak D.

Archivum Immunologiae et Therapiae Experimentalis

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2004

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vol. 52

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issue 6

447-456

EN

Previous ex vivo experiments by others suggest that elevated body temperature can prime the respiratory burst of human neutrophils. The mechanism of the priming phenomenon induced by temperature has not been addressed so far. Furthermore, the priming temperature range was not defined. In the present study we explored, under in vitro conditions, the influence of febrile.range temperatures on reactive oxygen species (ROS) generation by human peripheral blood neutrophils. ROS production was measured using whole.blood luminol.dependent chemiluminescence. Two elements of signal transduction pathways, calcium and p38 mitogen.activated protein kinase alpha (p38MAPK alpha), frequently underlying neutrophil priming were also examined. Calcium levels in the cytosol of resting and fMLP.stimulated isolated neutrophils were measured with the Fura.2AM spectrofluorimetric method. The activity of p38MAPK alpha was assessed indirectly with a specific inhibitor of the kinase, SB 203580. The study revealed a priming effect at 38?C toward human peripheral blood neutrophil ROS production. Any con. comitant effect on calcium response was not observed. Instead, experiments with SB 203580, a specific inhibitor of p38MAPK alpha, pointed to an increased activity of the kinase as a molecular background of temperature.induced priming. However, the priming effect of temperature was confined to 38?C, while higher temperatures proved to exert no effect (39 and 40?C) or even inhibited ROS generation by neutrophils (43?C). Our study suggests a heterogeneous influence of temperature on human neutrophil functioning, including the prim. ing of the cells by a low.febrile.range temperature. It also suggests a p38MAPK alpha dependent molecular background of the priming phenomenon.

16

Neutrophils in the innate immune response

71%

Kobayash S. D., Voyich J. M., Burlak C., DeLeo F. R.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 6

505-517

EN

Polymorphonuclear leukocytes (PMNs or neutrophils) are an essential component of the human innate immune system. Circulating neutrophils are rapidly recruited to sites of infection by host- and/or pathogen-derived components, which also prime these host cells for enhanced microbicidal activity. PMNs bind and ingest microorganisms by a process known as phagocytosis, which typically triggers production of reactive oxygen species and the fusion of cytoplasmic granules with pathogen-containing vacuoles. The combination of neutrophil reactive oxygen species and granule components is highly effective in killing most bacteria and fungi. Inasmuch as PMNs are the most abundant type of leukocyte in humans and contain an arsenal of cytotoxic compounds that are non-specific, neutrophil homeostasis must be highly regulated. To that end, constitutive PMN turnover is regulated by apoptosis, a process whereby these cells shut down and are removed safely by macrophages. Notably, apoptosis is accelerated following phagocytosis of bacteria, a process that appears important for the resolution of infection and inflammation. This review provides a general overview of the role of human neutrophils in the innate host response to infection and summarizes some of the recent advances in neutrophil biology.

17

Ischemia-reperfusion injury of the liver

71%

Ziaja J.

Postępy Higieny i Medycyny Doświadczalnej

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2001

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vol. 55

|

issue 3

433-448

EN

There is no single factor responsible for liver injury after its temporary ischemia and reperfusion. We deal with a mosaic of biochemical processes, in which a number of cells, mediators and enzymatic systems take part. The mechanism of liver injury remains far from full explanation.

18

Immunomodulatory role of the corticotropin releasing factor

71%

Radulovic M., Spiess J.

Archivum Immunologiae et Therapiae Experimentalis

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2001

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vol. 49

|

issue 1

33-38

EN

Corticotropin-releasing factor (CRF) was originally identified as a hypothalamic peptide which stimulates secretion of the hypophyseal adrenocorticotropic hormone. CRF exhibits its actions through G protein-dependent seven-membrane-domain receptors. Two subtypes of CRF receptors (CRFR1 and CRFR2) have been characterized thus far. CRF and its receptors were found in a number of brain regions, where they function by neuromodulation, and also in several peripheral organs. Besides CRF, another naturally occurring CRF-like peptide, urocortin, has been characterized. In the immune system, CRF and CRFR1 have so far been detected at both mRNA and protein lelvels in several lymphoid organs and at sites of inflammation. Locally injected CRF was shown to modulate the severity of inflammation. This effect was not only a result of hemodynamic changes known to be induced by CRF or by activation of the hypothalamo-pituitary adrenal axis, as CRF-binding sites were also found on immune cells. CRF was shown to directly modulate secretion of cytokines and neuropeptides, proliferation, chemotaxis and degranulation of purified macrophage and lymphocyte populations in vitro . The presence of functional CRFR was more recently demonstrated also on polymorphonuclear cells and significant amounts of CRF were shown to be produced in lymphoid organs, or delivered to lymphoid organs by peripheral nerves. Taken together, the experimental results obtained so far strongly point to the importance of CRF as a signaling molecule in lymphoid tissues and at the sites of inflammation.

19

Role of the p38 MAPK pathway in induction of iNOS expression in human leukocytes

71%

Jablonska E., Ratajczak W., Jablonski J.

Folia Biologica

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2008

|

vol. 56

|

issue 1-2

83-89

EN

Inducible nitric oxide synthase (iNOS) is one of the enzymes responsible for NO production in neutrophils (PMN) and in peripheral blood mononuclear cells (PBMC). Several studies have demonstrated that iNOS expression is controlled by a wide group of cytokines which achieve their biological effect through, among others, the activation of the p38 MAPK pathway. The aim of the present study was to define the participation of the p38 MAPK pathway in the induction of iNOS expression and NO production by PMN and PBMC of healthy persons after stimulation of rhIL-15 and rhIL-18. We also estimated the influence of rhIL-15 and rhIL-18 on cGMP production by both population cells and the production of superoxide anion radicals by neutrophils. The results show that rhIL-15 and rhIL-18 induced an increase in the expression of iNOS and phospho-p38 MAPK in PMN and PBMC. We also found that PMN and PBMC, stimulated by these cytokines, released larger amounts of NO and cGMP in comparison with non-stimulated cells. Additionally, PMN showed a more pronounced ability to produce superoxide anions. The results suggest that iNOS activation in neutrophils and in peripheral blood mononuclear cells stimulated with rhIL-15 and rhIL-18 may be achieved through the assistance of the p38 MAPK pathway.

20

Immunomodulation by alpha(1)-proteinase inhibitor: lack of chemotactic effects of recombinant human alpha(1)-proteinase inhibitor from yeast on human peripheral blood granulocytes

71%

Mosheimer B., Alzner R., Wiedermann C. J.

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2007

|

vol. 55

|

issue 6

399-403

EN

Introduction: Recombinant alpha(1)-proteinase inhibitor, clinically developed for inhalative augmentation therapy in patients with alpha(1)-proteinase inhibitor deficiency or cystic fibrosis, may directly contribute to leukocyte accumulation as it may function as a chemoattractant. The migratory effects of yeast-derived human recombinant alpha(1)-proteinase inhibitor on human peripheral blood neutrophils and eosinophils were therefore tested in vitro. Materials and Methods: Human peripheral blood leukocytes were prepared from forearm venous blood and tested for migration toward various preparations of yeast-derived recombinant alpha(1)-proteinase inhibitor in modified Boyden-chamber micropore filter assays. Results: No direct effects of yeast-derived recombinant human alpha(1)-proteinase inhibitor on in vitro migration of isolated neutrophils or eosinophils were seen. Conclusions: The lack of direct chemotactic effects of recombinant human alpha(1)-proteinase inhibitor despite anti-inflammatory effects in other biological activities of leukocytes may contribute to the preserved antibacterial defense mechanisms observed in patients under experimental augmentation therapy with inhaled alpha(1)-proteinase inhibitor.

Refine search results

Effect of IL-18 on IL-lbeta and sIL-1RII production by human neutrophils

Neutrophile activation by bacterial endotoxins

New biodefense strategies by neutrophils

Reactive oxygen intermediates and serum antioxidative system in patients with chronic C hepatitis treated with IFN-alpha and thymus factor X

TNF-alpha priming effect on polymorphonuclear leukocyte reactive oxygen species generation and adhesion molecule expression in hemodialyzed patients

Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

Regulation of the NADPH oxidase activity and anti-microbial function of neutrophils by arachidonic acid

Phagocyte NADPH oxidase: a multicomponent enzyme essential for host defenses

Effect of cardiopulmonary bypass on neutrophil activity in pediatric open-heart surgery

Neutrophil recognition of bacterial DNA and Toll-like receptor 9-dependent and independent regulation of neutrophil function

Granules of human neutrophils

Circadian variations of histamine binding to lymphocytes and neutrophils and skin reactivity to histamine in atopic and healthy subjects

Proinflammatory cytokine inhibitors, TNF- and oxidative burst of polymorphonuclear leukocytes in the pathogenesis of sepsis in newborns

iNOS expression and NO production by neutrophils in cancer patients

Temperature can prime human peripheral blood neutrophils in a p38MAPKa-dependent manner

Neutrophils in the innate immune response

Ischemia-reperfusion injury of the liver

Immunomodulatory role of the corticotropin releasing factor

Role of the p38 MAPK pathway in induction of iNOS expression in human leukocytes

Immunomodulation by alpha(1)-proteinase inhibitor: lack of chemotactic effects of recombinant human alpha(1)-proteinase inhibitor from yeast on human peripheral blood granulocytes