PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LEUKOCYTES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

From leukocyte reduction to leukocyte transfusion: the immunological effects of transfused leukocytes.

In transfusion medicine, mononuclear leukocytes have been studied more often as contaminants of red blood cells or platelets responsible for adverse transfusion outcomes than as therapeutic cells; leukocyte transfusion has been effective in augmenting recipient immunity only in limited clinical situations. Studies in leukocyte reduction and leukocyte transfusion have progressed separately as if the leukocytes' adverse and therapeutic effects result from different immunological mechanisms. With growing clinical experience, however, it is increasingly clear that some adverse immune effects may be exploited for therapeutic benefit. Advances in clinical immunology, understanding of the variety of cells and functions in the leukocyte fraction of blood, and blood component preparation technology may lead to new ways of deriving immunological benefit from transfused blood leukocytes while minimizing their adverse effects. This chapter reviews the current uses of leukocyte reduction and mononuclear leukocyte transfusion, with an emphasis on the relationship between transfusion-associated graft-versus-host disease and donor lymphocyte infusion in controlling relapsed leukaemias.

Antigen-Presenting Cells↗

Antigen-specific activity of murine leukocyte dialysates containing transfer factor on human leukocytes in the leukocyte migration inhibition (LMI) assay.

We report on the extension of the direct leukocyte migration inhibition (LMI) test as an assay for antigen-specific activity in human leukocyte dialysates (DLE) containing transfer factor to an evaluation of antigen-specific activity in DLE prepared from inbred mice. Murine DLE was observed to cause antigen-dependent and antigen-specific effects on the inhibition of migration of nonimmune human leukocyte populations. Pulsing of nonimmune human leukocyte with DLE preparations from BALB/c and SJL mice immunized with Candida, diphtheria toxoid, and SK-SD resulted in their inhibition of migration in the presence of the respective antigens. The antigen-specific activity in murine DLE was found to be present in lymph node cell preparations and to be absent from spleen cell preparations of the same donors. The activity of DLE in lymph node cells was found to be present in the theta-cell enriched subpopulation of nonadherent lymphocytes after passage through nylon wool columns. The antigen-specific activity of murine DLE, as we have reported for human DLE, was found to reside in the < 3500 dalton dialysis fraction and not in the < 3500 dalton fraction. We conclude that nonimmune human leukocytes in the LMI test provide a suitable assay for the detection of antigen-specific activity in murine DLE as well as that in human DLE. Additionally, murine DLE is active across species barriers and appears to share properties with human DLE.

Animals↗

Determination of leukocyte elastase-inhibitor complexes and leukocyte neutral proteinase inhibitor by enzyme immunoassays. Leukocyte elastase-inhibitor complexes in porcine blood, III.

Sensitive enzyme immunoassays for the determination of total leukocyte neutral proteinase inhibitor and polymorphonuclear elastase-leukocyte neutral proteinase inhibitor complexes are described. The usable ranges of the standard curves were from 80 ng/l to 10 micrograms/l. The relative intra-assay coefficients of variation of the tests were between 2 and 4%, and the inter-assay coefficients of variation between 4 and 10%. In vitro and in vivo studies were performed with septic pigs and isolated leukocytes. The results show that leukocyte neutral proteinase inhibitor can be used in pigs as a parameter for the development of a septicaemia.

Animals↗

LEUKOCYTES AND INTERFERON IN THE HOST RESPONSE TO VIRAL INFECTIONS. I. MOUSE LEUKOCYTES AND LEUKOCYTE-PRODUCED INTERFERON IN VACCINIA VIRUS INFECTION IN VITRO.

1. Investigation of the role of leukocytes in vaccinia virus infection is reported in an in vitro model, in the absence of an immune response. 2. Mouse leukocytes were shown to be capable of inhibiting the progression of vaccinia virus infection in primary mouse embryo fibroblast cultures. The degree of protection varied from slowing of spread of infection to complete control of the infection with eventual elimination of detectable virus and recovery of the culture. 3. Interferon production by leukocytes is thought to be an important factor in the observed protective effect.

Chick Embryo↗

Endothelial-leukocyte adhesion molecule-1-dependent and leukocyte (CD11/CD18)-dependent mechanisms contribute to polymorphonuclear leukocyte adhesion to cytokine-activated human vascular endothelium.

We have examined the contributions of endothelial-leukocyte adhesion molecule-1 (ELAM-1) and the complex of leukocyte surface adhesion molecules designated CD11/CD18 to the adhesion of human polymorphonuclear leukocytes (PMN) to cultured human endothelial cells (HEC), activated by rIL-1 beta for 4 or 24 h. Inhibition of PMN attachment to IL-1-activated HEC was measured in a quantitative in vitro monolayer adhesion assay, after treatment with mAb directed to ELAM-1 (mAb H18/17), and to CD11a (mAb L11), CD11b (mAb 44), CD11c (mAb L29), and CD18 (mAb 10F12), alone or in combination. Pretreatment of activated HEC with mAb H18/7 inhibited PMN adhesion by 47 +/- 8% whereas control mAb had no effect. CD11/CD18-directed mAb significantly blocked PMN adhesion to activated HEC (anti-CD11a, 40 +/- 3%; anti-CD11b, 34 +/- 4%; anti-CD18, 78+/- 6% inhibition). The combination of mAb H18/7 and each of the various anti-CD11/CD18 mAb resulted in greater inhibition of PMN adhesion than any Mab alone. After 24 h of rIL-1 beta treatment, when ELAM-1 was markedly decreased but elevated PMN adhesion was still observed, mAb H18/7 had no effect on PMN adhesion. At this time, CD11/CD18-dependent adhesive mechanisms predominated and a CD11c-dependent mechanism became apparent (anti-CD11a, 67 +/- 4% inhibition; anti-CD11b, 45 +/- 9%; anti-CD11c, 26 +/- 6%; anti-CD18, 97 +/- 1%). In summary, PMN adhesion to IL-1-activated HEC involves both CD11/CD18-dependent mechanisms and an ELAM-1-dependent mechanism, and the relative contribution of these varies at different times of IL-1-induced HEC activation. The additive blocking observed at 4 h with mAb H18/7 in combination with CD11/CD18-directed Mab implies that members of the CD11/CD18 complex do not function as an obligate ligand(s) for ELAM-1.

Antibodies, Monoclonal↗

Importance of L-selectin-dependent leukocyte-leukocyte interactions in human whole blood.

The objective of this study was to investigate whether leukocytes could be recruited by rolling leukocytes in a human whole blood model system. In all experiments, either neutrophils, whole blood, or diluted blood was perfused over immobilized E-selectin. With isolated neutrophils (2 x 10(5)/mL), the free-flowing neutrophils were captured by attached neutrophils to form secondary interactions that resulted in lines of rolling leukocytes. These secondary tethers accounted for 50% to 60% of all interactions and were eliminated by an L-selectin antibody, which also eliminated the lines of rolling leukocytes. Perfusion of whole blood or diluted blood revealed no lines of rolling leukocytes. The addition of red blood cells to isolated neutrophils either in a 1000:1 or a 10:1 ratio also inhibited lines of rolling leukocytes. Leukocytes were fluorescently labeled with rhodamine-6G so that leukocyte-leukocyte interactions could be studied in whole blood. A small number of secondary tethers (less than 20%) occurred and could be reduced by more than 80% with an L-selectin antibody. However, the overall impact on leukocyte recruitment was negligible. Similar experiments were performed using murine whole blood or isolated murine leukocytes. In the absence of red blood cells, murine leukocytes also formed lines of rolling leukocytes on E-selectin, and secondary tethers accounted for 50% of total interactions. However, when murine blood (diluted 1:5 with buffer) was perfused over E-selectin, secondary tethers accounted for only 13% of total interactions. These interactions were completely absent when blood was used from L-selectin-deficient mice. These data demonstrate for the first time that the importance of L-selectin-dependent leukocyte-leukocyte interactions is greatly reduced in whole blood and does not enhance overall recruitment of leukocytes in this physiologic milieu. (Blood. 2000;95:2954-2959)

Animals↗

Effects of Staphylococcus aureus on bovine mononuclear leukocyte proliferation and viability: modulation by phagocytic leukocytes.

In vitro effects of killed Staphylococcus aureus cells on bovine blood mononuclear leukocytes from uninfected cows or cows with chronic staphylococcal mastitis were assessed using a lymphocyte proliferation assay and a [51Cr] release cytotoxicity assay. Killed S. aureus cells cultured with mononuclear leukocytes caused a concentration-dependent decrease in lymphocyte proliferation that was associated with a concomitant decrease in mononuclear leukocyte viability. Responses of mononuclear leukocytes from uninfected and infected cows to killed S. aureus were similar, indicating effects were independent of the infection status of the animal. Addition of blood polymorphonuclear leukocytes to blood mononuclear leukocyte cultures without S. aureus cells did not alter mononuclear leukocyte viability but suppressed lymphocyte proliferation at the highest polymorphonuclear leukocyte:mononuclear leukocyte ratios (4:1 and 8:1) tested. When S. aureus cells and polymorphonuclear leukocytes were cultured with mononuclear leukocytes, both blood and milk polymorphonuclear leukocytes protected against the loss of viability compared with leukocytes cultured with S. aureus cells alone but did not consistently restore proliferative responses of the lymphocytes. These observations demonstrate that lymphocyte proliferation and mononuclear leukocyte viability are detrimentally affected by S. aureus cells, an effect that can be modulated by blood or milk polymorphonuclear leukocytes.

Animals↗

Leukocyte activation does not mediate myocardial leukocyte retention during endotoxemia in rabbits.

Our goal was to determine whether coronary leukocyte retention after endotoxin infusion was due primarily to leukocyte activation. Leukocytes were activated by infusion of endotoxin into 12 blood donor rabbits. Separately, 12 isolated rabbit hearts were perfused with blood from an endotoxemic support rabbit to expose coronary endothelium to an inflammatory stimulus. During an infusion of 20 ml of donor blood into the isolated heart, the coronary transit time of leukocytes was determined by deconvolution of multiple measurements of injectate and collected leukocyte concentrations. With no leukocyte activation or inflammatory stimulation of endothelium, leukocyte transit time was 9.2 +/- 3.5 s, and 11.6 +/- 4.1 x 10(6) leukocytes were retained in the coronary circulation. Leukocyte activation alone did not alter transit time (9.8 +/- 3.2 s) or retention (9.3 +/- 4.6 x 10(6) leukocytes). Inflammatory stimulation of endothelium with and without leukocyte activation increased transit time (18.0 +/- 3.6 and 18.9 +/- 3.8 s, respectively; P < 0. 05) and retention (24.8 +/- 8.4 and 25.3 +/- 6.8 x 10(6) leukocytes, respectively; P < 0.05) to the same extent. Differential counts showed that neutrophils (but not lymphocytes) were slowed and retained. Inflammatory stimulation of endothelium caused coronary capillary endothelial swelling and pseudopod formation. Thus increased coronary neutrophil transit time and retention are due to structural changes of coronary endothelial cells or other effects of the inflammatory response occurring within coronary capillaries, not only due to activation of leukocytes.

Animals↗

Inhibition of leukocyte locomotion by tocainide, a primary amine analog of lidocaine: at study with 111indium-labeled leukocytes and scanning electron microscopy.

The ability of tocainide (a primary amine derivative of lidocaine, 2-amino 2, 6-propionoxylidide) to inhibit leukocyte adhesion to and invasion of canine jugular veins was investigated. Leukocyte adhesion and migration were quantitated by use of 111indium-labeled leukocytes, and the morphologic characteristics of leukocytes and vessel lumen were studied by scanning electron microscopy. The morphologic characteristics of adhering and migrating 111indium-labeled leukocytes were similar to leukocytes that had not been manipulated, thus establishing their suitability for use as a marker for flammation. Exposure of leukocytes to 200 micrograms. per ml. of tocainide in autologous plasma in vitro inhibited adhesion and migration by 68 per cent. When labeled leukocytes were returned to the donor and exposed to intravenously infused tocainide the extent of reduction in adhesion and migration depended on whether tocainide infusion was started before or after neck dissection. Inhibition was only 46 per cent when dissection and injection of 111indium-labeled leukocytes preceded the start of infusion of tocainide but was 87 per cent when tocainide infusion was started before dissection and injection of leukocytes. The plasma level ranged from 25 to 47 microM over the 3 hour, 20 minute-infusion period, being 35 to 40 microM for the last hour. Migration of leukocytes across interendothelial junctions and their accumulation between the endothelial sheet and the basement membrane caused extensive damage to the endothelial lining of these veins. This was reduced when leukocyte migration was reduced. These observations suggest that the leukocyte-induced damage occurring in some sterile inflammations might be reduced by the use of local anesthetic drugs.

Anilides↗

Oxidative metabolism, cytoskeletal system, and calcium entry of leukocytes in the phenomenon of sensitizing cancer extract-induced leukocyte adherence inhibition.

We examined some of the metabolic events that regulate sensitizing cancer extract-induced leukocyte adherence inhibition and found that human leukocytes adhere in a comparatively passive manner to glass in serum-free medium. Adherence of leukocytes to glass did not require oxidative metabolism, microtubules, microfilaments, or calcium entry, whereas leukocyte mobility excited by sensitizing cancer extract did. Calcium antagonists, lanthanum chloride, cromolyn sodium, nifedipine, trifluoperazine, and lidocaine, prevented sensitizing cancer extract-induced leukocyte mobility. Calcium agonist, ionophore A23187, excited leukocyte mobility. Ouabain, which inhibits Na+-K+-adenosine triphosphatase and may increase intracellular Ca2+ as a result, also excited leukocyte mobility. Monocytes, armed with serum from patients with early cancer and challenged with the same sensitizing tumor antigen, generated a leukotriene mediator that excited leukocyte mobility; cromolyn sodium, nifedipine, and trifluoperazine antagonized the synthesis of the mediator. The calcium antagonists inhibited the leukotriene mediator and authentic leukotrienes B4, C4, and D4 from exciting leukocyte mobility. The results showed that leukocyte mobility, excited by sensitizing cancer extract, is an active process depending upon immunologically triggered release of a leukotriené mediator from armed monocytes. Leukocyte adherence inhibition requires many of the same physiological events that chemokinesis and chemotaxis do and is thus an assay to study either immunologically released chemoattractants or chemoattractants themselves on leukocyte locomotion.

Adenosine Triphosphate↗

Evidence in advanced cancer of an activated leukocyte state to explain the reversible defect in transmembrane signaling and leukocyte adherence inhibition to extracts of cancer.

When leukocytes bind tumor antigen, a transmembrane signal induces the cascade of physiological changes that result in leukocyte adherence inhibition (LAI). Leukocytes from patients with early stages of cancer exhibited transmembrane potential (delta psi) changes and LAI when incubated with a cancer extract of the same organ and histogenesis, whereas leukocytes from patients with advanced cancer did not. The refractoriness was reversed by transiently raising intracellular cyclic AMP. LAI is produced by leukotrienes and leukocytes from patients with advanced cancer were refractory to leukotriene-induced delta psi changes which was also restored by raising intracellular cyclic AMP. Moreover, leukocytes could be made refractory to delta psi changes: leukocytes from patients with early cancer when preincubated with a breast cancer extract showed no delta psi change with a second exposure; and leukocytes from control subjects preincubated with leukotrienes showed no delta psi change with a second exposure. The responsive population of leukocytes in LAI to either the specific cancer extract or leukotrienes consisted of about 35 to 42% of the adherent leukocytes. The responsive leukocytes in advanced cancer were already nonadherent, accounting for the 39% increased nonadherence with the control extract. Raising cyclic AMP decreased nonadherence by 39%. The results suggest that leukotrienes and other chemoattractants released in vivo by immune cells binding tumor antigen have stimulated the changes in leukocytes in advanced cancer. However, the unresponsiveness seems to be because of appropriate expression of physiological changes triggered by antigen and chemoattractant stimuli.

Breast Neoplasms↗

Liver ischemia/reperfusion induces an increase of microvascular leukocyte flux, but not heterogeneity of leukocyte trafficking.

Leukocytic response plays a major role in the manifestation of hepatic ischemia/reperfusion (I/R) injury. To clarify whether post-ischemic hepatic leukocyte accumulation is based on increased leukocyte flux to the hepatic tissue due to systemic inflammation or chemoattractant activities or whether it represents solely a local tissue response without changing overall leukocyte flux and trafficking characteristics through the microvasculature, we studied acinar and sinusoidal leukocyte flux and distribution in rat livers in vivo both under normal (sham, n = 8) and post-ischemic (60' ischemia/75' reperfusion) conditions (I/R, n = 8), using fluorescence epi-illumination microscopy (rhodamine-6G). Hepatic ischemia/reperfusion significantly (p < 0.05) increased acinar leukocyte flux (58.4 +/- 20.9 cells/min vs 36.4 +/- 12.8 cells/min in sham controls); however, it did not exhibit increased heterogeneity of acinar leukocyte distribution, as indicated by the unchanged coefficient of variance (CV) of 0.36 +/- 0.16 (sham controls: 0.31 +/- 0.14). In parallel, analysis of individual sinusoidal leukocyte flux demonstrated significantly (p < 0.05) higher values (8.9 +/- 3.7 cells/min) after ischemia/reperfusion when compared with sham controls (5.7 +/- 1.9 cells/min), which, however, was not associated with increased heterogeneity of sinusoidal leukocyte trafficking (CV: 0.85 +/- 0.15 vs 0.85 +/- 0.16 in sham controls) and manifestation of preferential pathways. Analysis of blood cell count did not demonstrate an overall increase of total blood leukocyte count; however, an increased (p < 0.01) fraction of polymorphonuclear leukocytes (65.2 +/- 11.2%) and stab cells (9.5 +/- 7.9%) during post-ischemic reperfusion when compared with sham controls (8.8 +/- 3.5% and 0.2 +/- 0.4%) was demonstrated. Thus, the increase of hepatic leukocyte flux after ischemia/reperfusion may be the result of both the manifestation of a systemic inflammatory response and the increase of local chemoattractant activities, such as the production and release of the cytokine-induced neutrophil chemoattractant of the IL-8 family.

Animals↗

Monoclonal antibodies to the leukocyte membrane CD18 glycoprotein complex and to intercellular adhesion molecule-1 inhibit leukocyte-endothelial adhesion in rabbits.

Increasing evidence indicates that leukocyte-endothelium adhesion is mediated, in part, by the CD11/CD18 family of heterodimeric glycoproteins expressed on the leukocyte plasma membrane and by intercellular adhesion molecule-1 (ICAM-1) which is expressed on endothelial cells. We have used the technique of intravital microscopy to visualize the microcirculation of the rabbit mesentery and to evaluate effects of antibodies against several adhesion glycoproteins on C5a-induced leukocyte adhesion. Addition of zymosan-activated serum (a source of C5a) to the buffer superfusing the mesenteric microvasculature induced rapid adhesion of leukocytes to the endothelium of post-capillary venules. Monoclonal antibodies R15.7 (anti-CD18), R7.1 (anti-CD11a, LFA-1), and R6.5 (anti-ICAM-1), administered intravenously before C5a exposure, strongly inhibited leukocyte adherence while antibody LM2 (anti-CD11b, Mac-1) produced significant, but weaker, inhibition. If these antibodies were administered after C5a-induced adhesion had begun, both R15.7 and R7.1 displaced adherent leukocytes and prevented further leukocyte accumulation: LM2 and R6.5 did not displace adherent leukocytes or inhibit incoming leukocytes from adhering. These data confirm earlier findings establishing a role for CD18 in leukocyte adhesion in vivo and extend those observations to implicate both CD11a and CD11b in that adhesion. In addition, we report that ICAM-1 mediates, in part, the initial leukocyte-endothelial cell adhesion following C5a exposure in vivo.

Animals↗

Transmembrane signal defect and absence of cancer extract induced leukocyte adherence inhibition (LAI) for leukocytes from patients with advanced cancer.

Leukocytes from patients with early cancer exhibit leukocyte adherence inhibition (LAI) when incubated with extracts of cancer of the same organ and histogenesis, whereas leukocytes from patients with advanced cancer seldom do. To understand the reason for this refractory state, tumor antigen-induced LAI and transmembrane signalling were measured in the same leukocytes. Transmembrane signalling was measured by changes in membrane potential (delta psi) by the [3H]tetraphenylphosphonium equilibration technique. When leukocytes from patients with early breast cancer were incubated with extracts of breast cancer and malignant melanoma they showed delta psi changes consisting of depolarization and hyperpolarization beginning within 0.5 min after addition of the breast cancer extract and finishing 15 min later. Moreover, they showed no delta psi changes when incubated with extracts of normal breast tissue. Leukocytes from subjects without cancer seldom showed delta psi changes. In criss-cross experiments, leukocytes from patients with melanoma only exhibited delta psi changes when incubated with the melanoma extract. There was a strong correlation between cancer extract-induced delta psi change and LAI. The delta psi change was triggered by leukotriene-like mediators from antibody-dependent monocytes. Authentic leukotrienes triggered delta psi changes in all subpopulation of leukocytes. Leukocytes from patients with advanced breast cancer when incubated with breast cancer extract did not transmit a signal or show LAI. Brief elevation of intracellular cyclic AMP restored both delta psi change and LAI induced by breast cancer extracts, indicating that reactive leukocytes are present but in a refractory state. We conclude that leukocytes from patients with advanced cancer do not react in LAI because tumor antigen does not trigger a transmembrane signal to initiate the cascade of biochemical reactions and physiological changes for LAI.

Breast Neoplasms↗

Scintigraphic assessment of leukocyte infiltration in acute pancreatitis using technetium-99m-hexamethyl propylene amine oxine as leukocyte label.

The infiltration of leukocytes has been linked to the pathophysiology of complicated or severe pancreatitis. We have tested the ability of leukocyte scintigraphy using technetium-99m-hexamethyl propylene amine oxine (HM-PAO) as label to demonstrate the localization of leukocytes in the pancreas during acute pancreatitis. Twenty-eight patients with acute pancreatitis (eight with biliary, 13 with alcoholic, and seven with unknown origin) were studied with leukocyte scintigraphy using planar imaging and single photon emission computed tomography (SPECT). Fourteen patients had a mild (group I), II a severe (group II), and three a lethal outcome (group III) of pancreatitis. All patients of group III, six of group II, and two of group I had a positive leukocyte scan. Thus, the sensitivity of leukocyte scintigraphy for the detection of a lethal course of acute pancreatitis was 100%, of a severe course 54%, and of a severe or lethal course 64%. The specificity of a negative scan for a mild pancreatitis was 86%. Comparison of the results of leukocyte scintigraphy with those of contrast enhanced CT showed that six of eight patients with pancreatic necrosis in CT had a positive leukocyte scan, but only five of 20 patients without detectable pancreatic necrosis in CT. In summary, leukocyte infiltration into the pancreas during pancreatitis can be demonstrated by noninvasive leukocyte scintigraphy using technetium-99m-HM-PAO as label. A correlation between the severity of the disease and leukocyte infiltration exists.

Acute Disease↗

Correlation of leukocyte adhesiveness, adhesion molecule expression and leukocyte-induced contraction following balloon angioplasty.

1. The aim of this study was to examine the changes in leukocyte adhesion and leukocyte-induced contraction in balloon-injured rabbit subclavian artery and to correlate these changes with vessel morphology and expression of adhesion molecules on the injured arteries. 2. Rabbits were anaesthetized and their left subclavian arteries were injured by balloon inflation and withdrawal followed by sacrifice at 2, 24, 48 h or 8 days after injury. The left and right subclavian arteries were removed and leukocytes were isolated from autologous rabbit blood. Leukocyte-induced contraction was measured in 5-HT precontracted artery rings and leukocyte adhesion was measured using (51)Cr-labelled leukocytes. Immunocytochemistry using paraffin-embedded tissue was employed to detect changes in the expression of adhesion molecules on injured arteries. 3. Autologous leukocytes caused a contraction of rabbit subclavian artery rings, which was prevented by L-NAME (10(-3) M). Balloon-induced injury abolished the contractile response to leukocytes, which correlated with loss of carbachol-induced relaxation 4. Balloon injury markedly enhanced the adhesiveness of the subclavian artery for leukocytes, most notably at 24 and 48 h after injury (1.7 and 1.8 fold respectively). Increased leukocyte adhesion at these two time points correlated with an upregulation of E-selectin, P-selectin and VCAM-1 expression on the remaining endothelium of the injured artery. 5. Vessel morphology revealed that balloon inflation had induced an infiltration of inflammatory cells into the vessel wall, the greatest increase being seen at 24 h after injury. 6. It is concluded that an increase in the expression of E-selectin, P-selectin and VCAM-1 following balloon-induced injury leads to enhanced leukocyte adhesion and migration into the injured vessel.

Angioplasty, Balloon↗

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↗