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PubMedDate not supplied

Ultrastructural damage of leukocytes procured by the Leukopak: vulnerability of leukocytes to mechanical injury.

Because of the often observed undesired effects in patients transfused with leukocytes collected by continuous filtration leukapheresis (CFL), we have investigated the morphology of these cells in the hope that such studies may help evaluate their in vivo functions. Aliquots of CFL samples, procured by the Fenwal Leukopak and taken before and after tapping the filters, were examined. Leukocytes prepared by dextran sedimentation served as controls and were used to demonstrate the vulnerability of these cells to mechanical injury. The morphology of leukocytes harvested by filtration leukapheresis was markedly altered, ranging from formation of cytoplasmic projections and vacuoles to disintegration of entire cells. The severe changes were only observed in samples collected after the filters were tapped. The number of cells involved varied from donor to donor. In some cases more than half of the examined leukocytes showed signs of damage. Dextran sedimentation leukocytes retained their normal ultrastructure. However, substantial injuries were inflicted on dextran sedimentation collected leukocytes following brief periods of vortexing. Our results indicate that leukocytes are quite vulnerable to mechanical injury, and the major cause of damage found in Leukopak-isolated leukocytes is the tapping of the filters. The toxic reactions in some recipients transfused with Leukopak-collected leukocyte preparations may result from materials released from disrupted leukocytes. We believe that the employment of the continuous filtration to procure leukocytes with the present procedure should be reviewed.

Blood Transfusion, Autologous↗
PubMed1996

Interactions through L-selectin between leukocytes and adherent leukocytes nucleate rolling adhesions on selectins and VCAM-1 in shear flow.

We demonstrate an additional step and a positive feedback loop in leukocyte accumulation on inflamed endothelium. Leukocytes in shear flow bind to adherent leukocytes through L-selectin/ligand interactions and subsequently bind downstream and roll on inflamed endothelium, purified E-selectin, P-selectin, L-selectin, VCAM-1, or peripheral node addressin. Thus adherent leukocytes nucleate formation of strings of rolling cells and synergistically enhance leukocyte accumulation. Neutrophils, monocytes, and activated T cell lines, but not peripheral blood T lymphocytes, tether to each other through L-selectin. L-selectin is not involved in direct binding to either E- or P-selectin and is not a major counterreceptor of endothelial selectins. Leukocyte-leukocyte tethers are more tolerant to high shear than direct tethers to endothelial selectins and, like other L-selectin-mediated interactions, require a shear threshold. Synergism between leukocyte-leukocyte and leukocyte-endothelial interactions introduces novel regulatory mechanisms in recruitment of leukocytes in inflammation.

Cell Adhesion↗
PubMed2006

PET with FDG-labeled leukocytes versus scintigraphy with 111In-oxine-labeled leukocytes for detection of infection.

PURPOSE: To compare prospectively the accuracy of positron emission tomography (PET) with leukocytes labeled in vitro with (18)F fluorodeoxyglucose (FDG) versus that of conventional scintigraphy with leukocytes labeled in vitro with (111)In oxine in patients suspected of having infection. MATERIALS AND METHODS: This HIPAA-compliant study had institutional review board approval; informed consent was obtained from all patients. Patients were 25 men and 26 women aged 32-86 years. In vitro labeling of autologous human leukocytes with FDG and (111)In-oxine was performed according to published methods. Labeling efficiencies and cell viability were determined. Imaging was performed 2.5-5.8 hours after injection of 196-315 MBq of FDG-labeled leukocytes and approximately 24 hours after injection of 17-25 MBq of (111)In-oxine-labeled leukocytes. Forty-three (20 men, 23 women; mean age, 59 years; range, 32-86 years) patients could be successfully imaged with both tracers. Six patients were not injected with FDG-labeled leukocytes because of low labeling efficiency (<35%). Two patients were injected with FDG-labeled leukocytes but were not imaged. One reader interpreted all results as positive or negative for infection. Imaging results were compared with final diagnoses. Labeling efficiencies and cell viabilities were compared by using the paired t test. Differences between PET and scintigraphy were determined by using the McNemar test. RESULTS: For the 43 patients who were imaged with both tracers, labeling efficiency of FDG was lower than that of (111)In oxine (72% +/- 8 [standard deviation] vs 90% +/- 5, P < .001). Viability of FDG-labeled leukocytes was not different from that of (111)In-oxine-labeled leukocytes (98% +/- 1 vs 97% +/- 3). There were no differences between FDG PET and (111)In scintigraphy in terms of sensitivity (87% vs 73%), specificity (82% vs 86%), or accuracy (84% vs 81%). CONCLUSION: PET with FDG-labeled leukocytes was comparable to scintigraphy with (111)In-oxine-labeled leukocytes. Further investigation in a larger population with dedicated PET or PET/computed tomography seems warranted.

Adult↗
PubMedDate not supplied

Cell adhesion molecules, leukocyte trafficking, and strategies to reduce leukocyte infiltration.

Leukocyte-endothelial cell interactions are mediated by various cell adhesion molecules. These interactions are important for leukocyte extravasation and trafficking in all domestic animal species. An initial slowing of leukocytes on the vascular endothelium is mediated by selectins. This event is followed by (1) activation of beta2 integrins after leukocyte exposure to cytokines and pro-inflammatory mediators, (2) adherence of leukocyte beta2 integrins to vascular endothelial ligands (eg, intercellular adhesion molecule-1 [ICAM-1]), (3) extravasation of leukocytes into tissues through tight junctions of endothelial cells mediated by platelet and endothelial cell adhesion molecule-1 (PECAM-1), and (4) perivascular migration through the extracellular matrix via beta1 integrins. Inhibiting excessive leukocyte egress and subsequent free radical-mediated damage caused by leukocyte components may attenuate or eliminate tissue damage. Several methods have been used to modify leukocyte infiltration in various animal models. These methods include nonspecific inhibition of pro-inflammatory mediators and adhesion molecules by nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, inhibition of cytokines and cytokine receptors, and inhibition of specific types of cell adhesion molecules, with inhibitors such as peptides and antibodies to beta2 integrins, and inhibitors of selectins, ICAMs, and vascular cell adhesion molecule-1 (VCAM-1). By understanding the cellular and molecular events in leukocyte-endothelial cell interactions, therapeutic strategies are being developed in several animal models and diseases in domestic animal species. Such therapies may have clinical benefit in the future to overcome tissue damage induced by excessive leukocyte infiltration.

Animal Diseases↗
PubMed1997

Amniotic fluid leukocytes and leukocyte esterase activity in parturients delivered by caesarean section.

Amniotic fluid specimens from parturients undergoing caesarean delivery were examined for leukocytes and leukocyte esterase activity, as well as for amniotic fluid bacteria and mycoplasmas by cultivation. The aim of this study was to evaluate the intrauterine environment in noninfected parturients and the associations between leukocyte test results, amniotic fluid microbial colonization and postcaesarean endometritis. Samples were obtained by direct aspiration at operation from 289 parturients with no clinical intrauterine infection. Among the total study population, leukocytes were found in 41% of the amniotic fluid samples by Gram staining and in 39% of the samples by the leukocyte esterase activity test. Leukocytes and leukocyte esterase activity were observed significantly more often in the amniotic fluids of parturients undergoing operation after onset of labour or ruptured membranes compared with those operated upon with intact membranes and no labour (p < 0.0001 and p < 0.0001). Of 255 amniotic fluid cultures, microbial colonization was observed in 82 (32%) parturients. Positive results in the leukocyte tests were associated significantly with amniotic fluid microbial colonization among parturients who underwent operation with intact membranes, or who underwent operation after rupture of the membranes and had cervical dilatation of < 5 cm at the operation (Gram stain: p < 0.0001; leukocyte esterase: p < 0.003). If cervical dilatation was > or = 5 cm, no such association was observed. In the population studied, endometritis developed in 2% and 4% of the parturients with positive test results. Thus, neither the presence of leukocytes nor detected leukocyte esterase activity were predictive of subsequent postoperative endometritis. In the detection of amniotic fluid microbial colonization, the tests functioned best in non-laboring parturients with intact membranes and in those operated on at the early stage of labour.

Adult↗
PubMed1975

An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization. II. Studies on the effect of leukocytic elimination on corneal vascularization.

Investigations on several experimental models in the past have supported the hypotheses that corneal vascularization is a manifestation of the inflammatory response and that leukocytes perform an essential role in stimulating corneal vascular ingrowth. To evaluate the possible role of leukocytes further in this phenomenon, the effect of leukocyte elimination on corneal vascularization induced by silver nitrate cauterization was investigated. Weanling Fischer albino rats received doses of total body x-irradiation ranging from 1100 to 2100 rads to deplete circulating leukocytes, and corneal silver nitrate cauterization was performed 4 days later. In this model, animals that received 1500 rads or more total body x-irradiation became severely leukopenic within 4 days. As a rule, neither leukocytes nor blood vessels invaded the cauterized corneas, whereas both a leukocytic and vascular invasion occurred at lower doses of irradiation that did not totally eliminate circulating leukocytes. Corneal vascularization ensued if the corneal cauterization was performed immediately after total body x-irradiation with 1500 rads before the leukopenic effect of x-irradiation occurred. Control studies in which the cornea was cauterized 4 days after only the head received 1500 rads x-irradiation ruled out the possibility of irradiation-induced limbal endothelial damage as the explanation for the vascular suppression observed by x-ray treatment. In nonirradiated rats, silver nitrate cauterization of the cornea consistently induced corneal vascularization by 2 to 3 days. In further experiments, methylprednisolone acetate was administered subconjunctivally after corneal cauterization. This corticosteroid inhibited the infiltration of leukocytes and the subsequent vascular invasion into the corneal stroma, if administered immediately after silver nitrate cauterization. However, when the same glucocorticoid was administered 1 day after cauterization, both a leukocytic infiltration and vascular ingrowth occurred but to a less severe degree than in non-glucocorticoid-treated cauterized corneas. These investigations together demonstrated that a vascular ingrowth of the cornea did not follow corneal cauterization with silver nitrate in the absence of leukocytes, and gives further support to the hypothesis that leukocytes serve a crucial function in corneal vascularization.

Animals↗
PubMed1990

Comparison of technetium-99m-HM-PAO leukocytes with indium-111-oxine leukocytes for localizing intraabdominal sepsis.

Technetium-99m-HM-PAO [( 99mTc]HM-PAO) leukocyte and indium-111-oxine (111In-oxine) leukocyte scanning were carried out simultaneously in 41 patients at 4 hr and 24 hr after reinjection to determine whether the 4-hr 99mTc scan could replace the 24-hr 111In scan for detecting intraabdominal sepsis. Abdominal infection was confirmed in 12 cases. The 4-hr 99Tc-leukocyte scan, the 4-hr 111In-leukocyte scan, and the 24-hr 111In-leukocyte scan yielded a sensitivity of 100%, 67%, and 100%, respectively, and a specificity of 62%, 90%, and 86%, respectively. The 24-hr 99mTc-leukocyte scan also produced a sensitivity of 100%, but it was falsely positive in all 29 cases without infection due to physiologic bowel uptake. False-positive 4-hr 99mTc-leukocyte scans were also produced by physiologic bowel uptake in seven cases all of whom had true-negative 4-hr and 24-hr 111In-leukocyte scans. Because of the high incidence of false-positive 4-hr [99mTc]HM-PAO leukocyte scans, it was concluded that they could not replace 24-hr 111In-leukocyte scans for detecting intraabdominal sepsis, and that serial 99mTc leukocyte scans starting earlier than 4 hr after reinjection must be evaluated.

Abdomen↗
PubMed1986

Leukocyte activation in advanced cancer as an explanation for absent leukocyte adherence inhibition to cancer extracts and chemoattractant.

Tube leukocyte adherence inhibition (LAI) measures human immunity by antigen-binding leukocytes releasing chemoattractant-like mediators that are the ultimate inhibitors of adherence by bystander leukocytes. We determined whether the absent LAI responses to cancer extracts for patients with large body burdens of bladder cancer was related to a defect in antigen binding or chemoattractant responsiveness. Leukocytes from patients with small body burdens of bladder cancer gave positive LAI responses of a similar extent to either bladder cancer extracts or chemoattractant [n-formyl-L-methionylleucylphenylalanine (FMLP)]. Of the adherent leukocytes, about 20-30% became non-adherent with a positive LAI response: monocytes, neutrophils and lymphocytes responded. In the control tubes, leukocytes from patients with large body burdens of bladder cancer were more non-adherent and about 15% less adherent than leukocytes from controls or patients with early cancer. They showed no further decrease in adherence, or conversely increase in non-adherence, with either extracts of bladder cancer or FMLP. The leukocytes also failed to transduce transmembrane signals to the same stimuli. The defect was reversible since PGE2 restored the adherence of leukocytes to normal, and subsequently they exhibited membrane potential changes and about 34% non-adherence to either bladder cancer extracts or FMLP. From these results we conclude that chemoattractant LAI-responsive leukocytes from patients with large body burdens of bladder tumor are activated in vivo, probably by mediators from inflammatory cells.

Cell Adhesion↗
PubMed2005

Intrauterine undernutrition in rats interferes with leukocyte migration, decreasing adhesion molecule expression in leukocytes and endothelial cells.

Experimental and epidemiologic data have shown that malnutrition predisposes individuals to infections. Immune responses are compromised, particularly in undernourished children. Therefore, we investigated the migratory capacity of leukocytes, using the intravital microscopy technique, in male Wistar rats (8-9 wk of age) that were undernourished in utero after their dams were fed 50% less food than the amount consumed by control dams. The number of leukocytes rolling along the venular endothelium, sticking after stimulation with leukotriene B4, tumor necrosis factor-alpha (TNF-alpha) or zymosan-activated plasma, or migrating after TNF-alpha stimulation was significantly reduced in the undernourished rat offspring. Compared with nourished rat offspring, undernourished offspring had significantly reduced numbers of circulating leukocytes, higher blood pressure, and higher leukocyte rolling velocity (V(WBC)), as well as a higher ratio between V(WBC) and RBC velocity (V(RBC)). Endothelial P-selectin and intercellular adhesion molecule-1 (ICAM-1) expression, analyzed by immunohistochemistry, and basal leukocyte L-selectin expression, analyzed by flow cytometry, were significantly reduced in the undernourished rat offspring. Because the groups did not differ in leukocyte CD11/18 expression, endothelial expression of platelet-endothelial cell adhesion molecule-1, or venular blood flow velocity and, consequently, venular shear rate, we conclude that intrauterine undernutrition in rats reduces leukocyte migration, downregulates endothelial expression of P-selectin and ICAM-1, as well as leukocyte expression of L-selectin, while reducing leukocyte counts. The higher V(WBC) and V(WBC)/V(RBC) ratio may also play a role in this reduced leukocyte migration. Our data suggest that this phenomenon is involved in the increased predisposition to infections in undernourished subjects.

Animals↗
PubMed2003

Reduction in shear stress, activation of the endothelium, and leukocyte priming are all required for leukocyte passage across the blood--retina barrier.

The passage of leukocytes across the blood-retina barrier at the early stages of an inflammatory reaction is influenced by a complex series of interactions about which little is known. In particular, the relationship between hydrodynamic factors, such as shear stress and leukocyte velocity, to the adherence and subsequent extravasation of leukocytes into the retina is unclear. We have used a physiological method, scanning laser ophthalmoscopy, to track labeled leukocytes circulating in the retina, followed by confocal microscopy of retinal flatmounts to detect infiltrating cells at the early stage of experimental autoimmune uveitis. This has shown that retinal vessels are subjected to high shear stress under normal circumstances. During the inflammatory reaction, shear stress in retinal veins is reduced 24 h before leukocyte infiltration. This reduction is negatively correlated with leukocyte rolling and sticking in veins and postcapillary venules, the sites of leukocyte extravasation. Activation of vascular endothelial cells is also a prerequisite for leukocyte rolling and infiltration. In addition, antigen priming of leukocytes is influential at the early stage of inflammation, and this is seen clearly in the reduction in rolling velocity and adherence of the primed leukocytes in activated retinal venules, 9 days postimmunization.

Animals↗
PubMed1985

Regulation of leukocyte glass adherence and tube leukocyte adherence inhibition (LAI) reactivity by serum factors in dogs with progressing or spontaneously regressing canine transmissible venereal sarcoma (CTVS).

We examined the regulation of leukocyte glass adherence and tube leukocyte adherence inhibition (LAI) reactivity by serum factors in dogs with regressing or progressing canine transmissible venereal sarcomas (CTVS). Both regressor and progressor peripheral blood leukocytes (PBL), draining and non-draining lymph node cells (LNC), and splenic leukocytes were significantly responsive to CTVS antigen extract in tube LAI. In contrast, a significant decrease in basal glass adherence of progressor PBL, draining and non-draining LNC, and splenic leukocytes was observed. Normal glass adherence was restored to progressor leukocytes by extensive washing with warm serum-free media, while significant tube LAI responsiveness to CTVS antigen extract was maintained. Preincubation of regressor PBL and LNC with progressor sera in two-stage tube LAI decreased the basal glass adherence of treated leukocytes. This effect of progressor sera was heat labile, a characteristic of CTVS antigen. Collectively, these findings suggest that progressor leukocytes and progressor sera treated regressor leukocytes were activated by interaction with serum CTVS antigen and thus behaved in tube LAI as stimulated cells, even in the absence of CTVS antigen. Regressor but not progressor sera were shown to contain anti-CTVS IgG with specific arming activity for normal dog PBL, but not LNC in two-stage tube LAI. The nonadherent response of peripheral blood neutrophils in two-stage tube LAI was proportional to the concentration of arming IgG, whereas no change was observed in glass adherence of PBL. The results of this study define the role of progressor and regressor serum factors in the mechanism of tube LAI and demonstrate a relationship between leukocyte glass adherence and the clinical course of CTVS. These findings show that tube LAI is a simple and reproducible measure of active factors in the immune response to a tumor.

Animals↗
PubMed2001

Soluble L-selectin at levels present in septic patients diminishes leukocyte-endothelial cell interactions in mice in vivo: a mechanism for decreased leukocyte delivery to remote sites in sepsis.

OBJECTIVE: Recent in vivo studies of both septic humans and animals demonstrate that leukocyte delivery is attenuated to sites remote from the primary infection. The mechanisms for this are not entirely clear. L-selectin is integral to rolling, the first step in leukocyte recruitment to an inflammatory site. L-selectin is shed from leukocytes in sepsis, resulting in increased levels of soluble L-selectin in plasma (2.33 microg/mL). This study investigates the effects of soluble L-selectin at levels found in sepsis on leukocyte trafficking in vivo. DESIGN: Prospective, controlled trial. SETTING: Surgical research laboratory in a university hospital. SUBJECTS: Swiss white male mice of 25-35 g. INTERVENTIONS: Mice were randomized to one of three study groups: soluble L-selectin 2.33, soluble L-selectin 8.0, or albumin. Intravital microscopy was performed on postcapillary venules of 20-40 microm in diameter in the cremaster muscle of mice. Leukocyte-endothelial cell interactions (rolling, adherence, and rolling velocity) were measured pre- and post- (1, 15, 30, and 45 mins) intravenous infusion of human recombinant soluble L-selectin (2.33 and 8.0 microg/mL) or human albumin (8.0 microg/mL). MEASUREMENTS AND MAIN RESULTS: The intravenous administration of soluble L-selectin to a systemic concentration of 2.33 microg/mL diminished rolling significantly. Soluble L-selectin at 8.0 microg/mL decreased rolling and increased rolling velocity to a greater degree. Injection of albumin did not alter leukocyte-endothelial cell interactions at any time point. No difference between groups in blood pressure, shear rate, or leukocyte counts was detected. CONCLUSIONS: Soluble L-selectin diminishes leukocyte rolling at levels present in sepsis (2.33 microg/mL). This effect is dose dependent, and could not be explained by differences in blood pressure, shear rate, or leukocyte counts. These findings identify increased soluble L-selectin levels as one of the mechanisms for decreased leukocyte delivery and exudation to remote sites in septic patients.

Analysis of Variance↗
PubMed2002

Activated polymorphonuclear leukocytes enhance production of leukocyte microparticles with increased adhesion molecules in patients with sepsis.

BACKGROUND: Leukocyte microparticles (MPs) derived from polymorphonuclear leukocytes (PMNLs) have been recently found to be activators of vascular endothelium in vitro. The precise role of leukocyte MPs has not been clarified in patients suffering severe insult. The objective of this study was to evaluate production of leukocyte MPs and expression of adhesion molecules on the MP surface in patients with sepsis. METHODS: Twenty-one patients with severe infection (fulfilling the criteria of sepsis with serum C-reactive protein > 10 mg/dL) and 21 healthy volunteers were included as study subjects. Production of leukocyte MPs, expression of CD11b on the MPs, and oxidative activity of PMNLs were measured by flow cytometry in the presence and absence of formyl-methionyl-leucyl-phenylalanine. CD11b expression was evaluated according to the MP size (more than, equal to, or less than 1.0 microm). Soluble E-selectin, thrombomodulin, and PMNL elastase were also measured in blood. RESULTS: Production of leukocyte MPs and superoxide production in PMNLs with and without formyl-methionyl-leucyl-phenylalanine increased significantly in patients with sepsis in comparison with production in normal volunteers. In patients with sepsis, expression of CD11b was also markedly enhanced on MPs less than 1.0 microm in diameter in comparison with expression in control subjects. Levels of soluble E-selectin, thrombomodulin, and PMNL elastase in blood were significantly increased in patients with sepsis. We succeeded in detecting leukocyte MPs visually by fluorescence microscopy. CONCLUSION: Activated PMNLs enhance production of leukocyte MPs with increased adhesion molecules in patients with sepsis. Activated leukocyte MPs may play a role in the pathogenesis of endothelial activation and leukocyte-endothelium interaction in the presence of sepsis.

Adult↗
PubMed2000

Evaluation of leukocyte dynamics in choroidal circulation with indocyanine green-stained leukocytes.

PURPOSE: To develop a new method with which to visualize leukocytes moving through the choroidal vessels of pigmented animals and enable the evaluation of leukocyte dynamics in the choroidal microcirculation. METHODS: Pigmented rabbits and monkeys were used in this study. Leukocytes, collected by centrifugal separation of autologous blood, were stained with indocyanine green (ICG) dye. The ICG-stained leukocyte fluid was injected into the vein, and the fundus image was obtained with a scanning laser ophthalmoscope. The image was recorded on videotapes and analyzed with a personal computer-based image analysis system. RESULTS: In pigmented rabbits, fluorescent leukocytes moving in the choroidal circulation were clearly visible for more than 1 hour. In monkeys, distinct fluorescent dots were seen moving approximately 50 to 200 microm in the foveal avascular zone for more than 30 minutes after the injection of the ICG-stained leukocyte fluid. Dim fluorescent dots were seen moving in the fundus. Although the movement of these dim dots was difficult to trace, they seemed to be moving in the choroidal vessels. In the rabbits, the mean flow velocity of leukocytes moving without plugging was 0.48 +/- 0.14 mm/sec in the peripheral choriocapillaris. In the monkeys, the mean flow velocity of distinct fluorescent leukocytes without plugging was 2.45 +/- 0. 48 mm/sec in the posterior choroid. CONCLUSIONS: In pigmented rabbits and monkeys, this method allows visualization of leukocytes passing through the choroidal vessels and provides a new way to investigate, noninvasively and in vivo, leukocyte dynamics in the choroidal microcirculation.

Animals↗
PubMed1997

Leukocyte migration in acute colonic inflammatory bowel disease: comparison of histological assessment and Tc-99m-HMPAO labeled leukocyte scan.

UNLABELLED: Noninvasive leukocyte scintigraphy for assessment of localization, extent, and degree of active inflammation in acute colonic inflammatory bowel disease have been shown to correlate well with endoscopy. This study compared findings of mucosal leukocyte migration assessed histologically with those of technetium 99m hexamethylpropylene-amineoxime-labeled leukocyte scintigraphy. PATIENTS AND METHODS: Twenty-one patients hospitalized because of a first attack or a relapse of known inflammatory bowel disease were investigated using leukocyte scintigraphy followed by total colonoscopy with multiple biopsies within 24 h. Histological interpretation focused on the degree of segmental mucosal leukocyte infiltration. RESULTS: Fourteen patients with ulcerative colitis (UC) and seven with colonic Crohn's disease (CD) were included. With the use of histology as the reference method, maximal proximal disease extent was correctly assessed by the leukocyte scan in 11 patients (8 with UC, 3 with CD), although the rectal involvement was not visualized in 5. In seven patients, the extent assessments almost matched (+/- one segment), and in the remaining three patients (two UC, one CD) the scan grossly misinterpreted active histological inflammation (> or = +/- two segments). In patients with UC, the sensitivity, specificity, and diagnostic accuracy concerning the extent of inflammation were 0.84, 0.79, and 0.83, respectively. In patients with CD, the sensitivity was 0.79, and the diagnostic accuracy was 0.78. The relative leukocyte scan activity score was less concordant with the degree of mucosal leukocyte infiltration but still significantly correlated (r = 0.616, p < 0.0001 in UC patients and r = 0.441, p < 0.003 in CD patients). CONCLUSION: Images created by the technetium 99m hexamethylpropylene-amineoxime-labeled leukocyte scan in acute colonic inflammatory bowel disease correlate to mucosal leukocyte migration in terms of proximal disease extent and, to a lesser degree, also to the intensity of mucosal inflammatory infiltration.

Acute Disease↗
PubMedDate not supplied

Leukocytes-depleting filters preferentially remove activated leukocytes and reduce the expression of surface adhesion molecules during the simulated extracorporeal circulation of human blood.

The effect of leukocyte-depleting filters on the total and activated leukocyte counts and the expression of surface adhesion molecules CD11b, CD18, and CD62L during the in vitro extracorporeal circulation of human blood was studied. A 200 ml blood sample was taken from 10 patients undergoing CABG surgery. The blood was circulated for 60 minutes within an experimental extracorporeal circuit. A leukocyte-depleting filter was attached in five circuits (filtered group). In five other circuits, no filter was used (controls). Total leukocyte counts were determined manually. Activated leukocytes were identified using nitroblue tetrazolium staining. The expression of CD11b, CD18, and CD62L was measured with flow cytometry. At 60 minutes, total leukocyte counts were reduced by 49% from the baseline values in the filtered group and 10% in the control group (p < 0.0001). Activated leukocyte counts decreased by 86% in the filtered group and increased by 116% in the control group (p < 0.0001). In the filtered group, the expression of CD11b, CD18, and CD612L decreased by 60%, 21%, and 79%, respectively, and in the control group it increased by 24%, 6%, and 28% (p < 0.0001). Leukocyte-depleting filters preferentially remove activated leukocytes and reduce the expression of CD11b, CD18, and CD62L during the in vitro extracorporeal circulation of human blood.

Aged↗
PubMed2004

Chronic blockade of nitric oxide biosynthesis in rats: effect on leukocyte endothelial interaction and on leukocyte recruitment.

INTRODUCTION: Previous studies showed that animals chronically treated with NG-nitro-L-arginine methyl ester (L-NAME) have a reduced inflammatory reaction. Now the role of L-NAME treatment (20 mg/Kg/day/14 days) on leukocyte mobilisation was assessed in rats. METHODS: In vivo leukocyte recruitment evoked by Bothrops jararaca venom (BjV) and nitrite/nitrate (NO2-/NO3-; Griess reaction) were evaluated in the air pouch cavity. Haematological parameters were evaluated in the bone marrow and in the peripheral compartment. Microcirculatory blood flow, number of rolling and adhered leukocytes, vascular reactivity and mast cell activity were studied by intravital microscopy. Blood pressure was measured by the tail-cuff method. L-selectin and beta(2) integrin expressions on peripheral and bone marrow leukocytes were quantified by flow cytometry. RESULTS: When compared with control rats (D-NAME) L-NAME treated rats had reduced PMN cell infiltrate (50%) and NO2-/NO3- (27%) in the air pouch cavity. Rolling leukocytes were decreased (70%) in L-NAME-treated animals, which was reversed by topical application of NO donor (SIN-1). BjV stimulation increased the number of rolling and adhered leukocytes only in control rats. Systemic blood pressure, microcirculatory blood flow and microvascular reactivity was not altered by the treatment. Only the vessel response to acetylcholine was delayed in treated rats. Peripheral PMN cells were increased by L-NAME treatment (100%), but the number of bone marrow cells was not altered. The treatment reduced L-selectin expression on circulating leukocytes, by either with (16%) or without (26%) stimulation with BjV; PMN cells were more affected (32-37%). Impairment of L-selectin expression was also verified in bone marrow cells under stimulation with BjV. CONCLUSIONS: Results show that this schedule of L-NAME treatment promotes a decrease on L-selectin expression. This effect may promote the standstill of leukocytes in the blood compartment and may be responsible, at least in part, for the observed deficient leukocyte-endothelium interactions with subsequent impairment of leukocyte migration to the inflammatory site.

Animals↗
PubMed1984

Antigen-independent leukocyte random locomotion inhibitory activity in human ultrafiltrated leukocyte extracts.

Human ultrafiltrated leukocyte extracts (MW less than 5000) were fractionated by Sephadex G-10 column chromatography and the effects of these fractions on leukocyte random locomotion were investigated in vitro. Fr-4, one of these fractions, had significant leukocyte random locomotion inhibitory activity, independent of the presence of mononuclear leukocytes. This inhibitory activity was not due to cytotoxic effects on leukocytes. As seen by scanning electron microscopy, the number of cell surface pseudopods on leukocytes incubated with Fr-4 was reduced. Fr-4A, one of three fractions separated from Fr-4 by Sephadex G-25 column chromatography, significantly inhibited leukocyte random locomotion. Fr-4A contained numerous components, one of which was identified as 2-deoxyribose, on the basis of thin-layer chromatography. Biologically 2-deoxyribose showed an inhibitory effect on leukocyte locomotion and a reduction of the extrusion of pseudopods on the surface of leukocytes, at the range of assayed concentrations. This inhibitory activity is probably derived from 2-deoxyribose.

Antigens↗