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PubMedDate not supplied

Model studies of leukocyte-endothelium-blood interactions. II. Hemodynamic impact of leukocytes adherent to the wall of post-capillary vessels.

Computational fluid dynamics (CFD) and large scale model experiments were used to analyze the hemodynamic impact of leukocytes adherent to the wall of post-capillary venules. Using a large scale model and, with the aid of a finite element package, solving the Navier Stokes equations for low Reynolds number flow in a cylinder past an adherent sphere, we have developed a dimensionless correlation which permits the estimation of the pressure drop across an adherent leukocyte in an in vivo vessel. This relationship is: f.Re = exp[2.877+4.630 (d/D)4] where f is the Fanning friction factor, Re is the Reynolds number and d/D is the leukocyte to vessel diameter ratio. The friction factor is proportional to the pressure drop across the leukocyte, and does not significantly increase until d/D is greater than 0.5, and then increases rapidly with increasing d/D. Computations indicate that the length of the disturbed flow region generated by an adherent leukocyte increases with decreasing vessel size. The average wall stress in the disturbed flow region remains constant, and equal to the wall stress in the undisturbed region for d/D less than approximately 0.5. For d/D greater than 0.5, the average wall stress in the disturbed flow region increases rapidly with increasing d/D. There is an even larger increase, up to five times greater than the average disturbed stress, in the peak wall stress in the disturbed flow region. This indicates that significant wall stress gradients can be generated by an adherent leukocyte in post-capillary size vessels.

Cell Adhesion↗

PubMed1994

Peripheral leukocyte count and leukocyte indexes in healthy newborn term infants.

PURPOSE: This study was designed to determine normal values for the peripheral leukocyte count and leukocyte indexes in healthy term neonates at a specific time after birth. METHODS: We prospectively enrolled 193 healthy term-gestation neonates with no identifiable perinatal risk factors for sepsis. At 4 hours of age a blood sample was collected by warmed heel stick. An automated Coulter complete blood cell count and a 100-cell manual differential leukocyte count were performed on each sample. The differential count was performed by a single hematopathologist unaware of the clinical status of each infant. Perinatal factors were identified by review of the mothers' and infants' hospital records. RESULTS: The mean ratio of immature to total neutrophils was 0.16 (SD 0.10), and the 10% to 90% range was 0.05 to 0.27. The mean leukocyte count was 24.06 x 10(9)/L (24,060/mm3), and the 10% to 90% range was 16.2 to 31.5 x 10(9)/L (16,200 to 31,500/mm3). Neutropenia, < 1.5 x 10(9)/L (1500/mm3) segmented plus band form neutrophils, was not observed. Of all the perinatal factors studied, only the duration of stage 1 labor was found to be associated with significant elevations in the leukocyte and absolute neutrophil counts. CONCLUSIONS: Previously published normal ranges for leukocyte indexes in healthy newborn infants during the early neonatal period are too restrictive; reference standards should be broadened.

Blood Cell Count↗

PubMed2006

Conversion of the severe to the moderate disease phenotype with donor leukocyte microchimerism in canine leukocyte adhesion deficiency.

Leukocyte adhesion deficiency-1 (LAD-1), a genetic immunodeficiency disease characterized by life-threatening bacterial infections, results from the defective adherence and migration of leukocytes due to mutations in the leukocyte integrin CD18 molecule. Canine LAD (CLAD) represents the canine homologue of the severe phenotype of LAD-1 in children. In previous studies we demonstrated that non-myeloablative stem cell transplantation from matched littermates resulted in mixed donor-host chimerism and reversal of the disease phenotype in CLAD. In this study, we describe two CLAD dogs with less than 2% donor leukocyte chimerism following non-myeloablative transplant. Both dogs are alive more than 24 months after transplant with an attenuated CLAD phenotype resembling the moderate deficiency phenotype of LAD. The improvement in the CLAD phenotype with very low levels of donor CD18(+) leukocytes correlated with the preferential egress of the CD18(+) neutrophils into extravascular sites. The clinical response with very low levels of donor CD18(+) leukocytes in CLAD supports using this model for testing gene therapy strategies since the low levels of gene-corrected hematopoietic cells expected with hematopoietic gene therapy would likely have a therapeutic effect in CLAD.

Animals↗

PubMed1975

The effect of leukocyte hydrolases on bacteria. III. Bacteriolysis induced by extracts of different leukocyte populations and the inhibition of lysis by macromolecular substances.

The lysis of 14C-labeled bacteria by hydrolases of human and rabbit leukocytes was studied in vitro. While Staphylococcus albus, Streptococcus faecalis, and Streptococcus mutans were highly susceptible to lysis, Staphylococcus auresus was intermediate in its susecptibility to lysis by the leukocyte enzymes. Group A Streptococcus, Listeria monocytogenes, Shigella flexneri, Escherichia coli, and Mycobacterium smegmatis were very resistant to degradation by these enzymes. The lytic activity of leukocyte lysates from human and rabbit blood was probably due to acid hydrolases of polymorphonuclear leukocytes. Extracts of human blood monocytes and of rabbit peritoneal and lung macrophages were less lytic for the bacteria tested. Lymphocytes and platelet extracts were not bacteriolytic. The lytic effect of the leukocyte lysates was not inhibited by KCN or sodium azide, but was abolished to a large extent by cationic polyelectrolytes such as protamine sulfate, histone and leukocyte cationic proteins, and poly-lysine, as well as by the anionic polyelectrolytes such as heparin, chondroitin sulfate, DNA, carrageenin, alginate sulfate, dextran sulfate, and ploy-L-glutamic acid. Other potent inhibitors of bacteriolysis were trypan blue, congo red, phosphatidic acid, normal immunoglobulins, and components of streptococcal cell wall.

Animals↗

PubMed1978

Neutralizing antibodies against human leukocyte, lymphoblastoid and fibroblast interferons elicited by immunization with human leukocyte interferon.

Guinea pigs, rabbits, and sheep were immunized with partially purified human leukocyte interferon. The antisera were tested for their neutralizing activities against human leukocyte, lymphoblastoid (Namalva) and fibroblast interferons. Rabbits and sheep developed high levels of neutralizing antibodies against all three interferons. The ratios of the neutralizing activities of leukocyte/lymphoblastoid interferons varied from 1 to 25 and those of leukocyte/fibroblast interferons from 2 to 500. The ratios increased with prolonged immunization. The guinea pigs developed relatively low levels of anti-leukocyte and anti-lymphoblastoid antibodies and as a rule failed to produce detectable neutralizing activity against fibroblast interferon. One sheep was given a booster injection of fibroblast interferon after preimmunization with leukocyte interferon. The booster injection stimulated a rise in antibody levels, not only for fibroblast interferon, but also for leukocyte and lymphoblastoid interferons. The antigenic relationships between leukocyte, lymphoblastoid and fibroblast interferons are discussed.

Animals↗

PubMed1997

Strategy of leukocyte filtration for immunomodulation: development of stainless steel leukocyte filter.

Commercially available leukocyte filters are frequently used to prepare leukocyte depleted blood products for prevention of transfusion reactions. Recently, immunomodulation by using leukocyte filtration was evaluated. At this time, a new leukocyte filter was fabricated with a 4 microm diameter stainless steel fiber. The goal of this study was to assess the efficiency of the stainless steel filter for leukocyte and platelet removal by comparison with the polyester filter that is commercially available. The production of humoral factors, including interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-1 receptor antagonist (IL-1 Ra), was also evaluated. The results show that the stainless steel filter has more than 2 times greater efficiency in leukocyte removal than the polyester filter. Furthermore, the cytokine studies indicate good biocompatibility of the filter, and the stainless steel filter has a possibility of inhibiting inflammatory cytokines by inducing interleukin-1 receptor.

Antibody Formation↗

PubMed1998

Platelet-leukocyte activation during hemodialysis detected with a monoclonal antibody to leukocyte integrin CD11b.

Platelet activation is commonly monitored with a battery of monoclonal antibodies against different platelet epitopes with controversial results. The transient expression of platelet markers and their role mediating interactions with other cells could easily explain these discrepancies. The present study has evaluated whether the analysis of a leukocyte activation antigen (CD11b) could provide more reliable results than detection of platelet activation markers. Cytometric techniques with specific monoclonal antibodies were used to compare the reliability of platelet and leukocyte markers to detect activation. Modifications in the presence of platelet glycoproteins GPIb (CD42b), GPIIIa (CD41) and GPIV (CD36), expression of specific platelet markers (P-selectin (CD62P) and lysosomal protein (CD63)) and leukocyte integrin (CD11b) were assessed during hemodialysis. Platelet antigens remained in uremic patients at levels similar or slightly above those detected in a group of healthy subjects. Modifications of platelet antigens during hemodialysis produced inconclusive results. However, numbers of leukocytes expressing CD11b increased progressively during hemodialysis (17.2 +/- 5.1% at 15 min and 21.3 +/- 6.6% at 2 h, p < 0.05, vs. baseline 6.9 +/- 0.2%). The hemodialysis procedure caused an increased formation of leukocyte-platelet aggregates. Detection of leukocyte CD11b may be a useful marker of overall cellular activation during the hemodialysis procedure.

Aged↗

PubMed1969

The enzymatic mechanisms for deoxythymidine synthesis in human leukocytes. IV. Comparisons between normal and leukemic leukocytes.

(1) Synthesis of deoxythymidine by either direct transfer of deoxyribosyl to thymine (pyrimidine deoxyribosyltransferase) or by a coupled deoxynucleoside phosphorylase mechanism is approximately twofold greater with normal leukocyte extracts (55 to 88% granulocytes) than with extracts prepared from leukocytes obtained from patients with chronic myelogenous leukemia. Activities in lymphocytes (normal or leukemic) are one-fifth the activity of normal granulocytes.(2) The lower activity in chronic myelogenous leukemia remains at 50% of normal even when patients are in hematologic remission with a normal per cent mature granulocytes in the peripheral blood.(3) The leukemic enzyme could not be distinguished from the normal by pH optima, thermal stability, or kinetic properties. The Km's for the deoxyribosyl acceptor and deoxyribosyl donors were identical for both enzymes. Both are subject to substrate inhibition by thymine and to inhibition by purine bases with similar Ki's. In addition, the transferase component of both the leukemic and the normal cell enzyme is activated by phosphate and arsenate. It appears, therefore, that there is no qualitative difference between the enzyme obtained from leukocytes of patients with chronic myelogenous leukemia and the enzyme obtained from normal leukocytes, suggesting that the difference in total cell activity is due to an actual decrease in amount of enzyme in chronic myelogenous leukemia or to a mixed cell population, one with a normal quantity of enzyme and the other with little or no active enzyme.(4) In both the normal cell and the leukemic cell extracts, transferase and phosphorylase activities could not be separated. The ratio of the two activities remained constant over a 140- and a 230-fold purification in normal and leukemic cell extracts, respectively. These and other observations indicate that transferase and phosphorylase activities are associated with the same protein.(5) The metabolism of pyrimidine and purine deoxynucleosides is similar for normal and leukemic cells. Catabolism of all deoxynucleosides tested was by direct phosphorolysis, except for deoxyadenosine which required initial deamination to deoxyinosine before phosphorolysis. In contrast to the greater rates of pyrimidine deoxynucleoside synthesis and cleavage with normal leukocyte extracts, the rates of purine deoxynucleoside synthesis and cleavage were approximately twofold greater with extracts prepared from cells of patients with chronic myelogenous leukemia. There was no significant difference in the rate of phosphorolytic cleavage of pyrimidine nucleosides (uridine) between the CML and normal leukocyte extracts.

Glucosyltransferases↗

PubMed1990

The role of leukocyte depletion by in vivo use of leukocyte filter in lung preservation after warm ischemia.

The oxygen metabolites of leukocytes have been implicated as playing the central role in reperfusion injury of preserved lung for transplantation. Furthermore, it is still unknown how leukotrienes take part in this process. Twelve mongrel dogs were used, divided into two groups. In group A, left thoracotomy and hilar stripping of the left lung was performed under anesthesia. During warm ischemia (two hours) and reperfusion (two hours), a filter was used three times between the femoral artery and vein, and quantitative in vivo blood filtration was performed. In group B, warm ischemia and reperfusion was done in the same fashion without filtration. As for tissue free radical assay, lipid peroxidation products were measured by means of thiobarbituric acid. Tissue leukotriene B4 and C4 levels were measured by radio immunoassay. In addition, peripheral blood count and tissue wet/dry ratio were analyzed. Significant leukocyte depletion of peripheral blood with leukocyte efflux from reperfused lung was observed in group A. Significant increase of tissue malondialdehyde (MDA) titers after reperfusion was observed in group B, whereas no significant fluctuation of tissue MDA titers was noted in group A. Concerning leukotriene B4 and C4, no significant increase was observed in either group. Tissue damage estimated by lung wet/dry ratio was considered to be controlled in group A compared with group B. Thus, the authors conclude that in vivo use of a leukocyte filter is efficient in removal of peripheral blood leukocytes and in preservation of reperfused lung after warm ischemia and that oxygen metabolites of leukocytes are considered to play a role in tissue damage in this process.

Animals↗

PubMed2006

Platelet activation, upregulation of CD11b/ CD18 expression on leukocytes and increase in circulating leukocyte-platelet aggregates in Indian women chronically exposed to biomass smoke.

The majority of households in rural India still rely on unprocessed solid biomass for domestic energy. The aim of this study was to investigate whether chronic exposure to biomass smoke causes activation of leukocytes and the formation of leukocyte-platelet aggregates. We conducted flow cytometric analysis of beta2 Mac-1 integrin (CD11b/CD18) expression on polymorphonuclear leukocytes (PMN) and monocytes, and P-selectin (CD62P) expression on the platelets of 165 women from eastern India, who cook solely with wood, dung and agricultural wastes, and 155 age- and socio-economic condition-matched control subjects, who used relatively cleaner fuel, liquefied petroleum gas (LPG). Leukocyte-platelet aggregates were defined as CD11b-positive PMN and monocytes co-expressing platelet-specific markers CD41 or CD62P. A significant increase in leukocyte-platelet aggregates was found in women who used biomass as cooking fuel. In addition, they showed increased surface expression of CD11b/CD18 in circulating PMN and monocytes and CD62P expression on platelets. The mean fluorescence intensity (MFI) of CD11b on the surface of circulating monocytes and PMN of biomass users increased by 50 and 68%, respectively. Similarly, a 62 and 48% increase in MFI was observed in CD18 expression on the surface of these cells in biomass users. The results show that chronic biomass smoke exposure activates circulating platelets, PMN and monocytes, and increases the number of leukocyte-platelet aggregates, which are considered a risk factor for thrombosis.

Adult↗

PubMed1996

Human myeloblastin (leukocyte proteinase 3): reactions with substrates, inactivators and activators in comparison with leukocyte elastase.

Human myeloblastin (leukocyte proteinase 3) shares many biochemical properties with leukocyte elastase, but rapidly loses enzymatic activity when raising the pH and/or the ionic strength of an acidic solution or when handled in glass vessels. This poses limits to kinetic experiments requiring long incubation times. After purification, myeloblastin was conveniently stored in a glycine/HCl buffer at pH 3.2, while assays were performed in sodium/potassium phosphate buffer at pH 7.0, ionic strength 0.11, in the presence of 0.05% w/v Triton X-100 and taking care to avoid any contact with glass surfaces. The kinetic parameters of leukocyte elastase and myeloblastin with peptide substrates, irreversible inactivators and glycosaminoglycans were compared under these conditions. MeO-succinyl-Lys(2-picolinoyl)Ala-Pro-Val-4-nitroanilide, an excellent substrate for leukocyte elastase, also proved to be a good substrate for myeloblastin (Km = 16 microM, kcat/Km = 30,600 M(-1)s(-1)). Inactivation of myeloblastin by 3,4-dichloroisocoumarin (ki/Ki = 6,389 M(-1)s(-1)) and MeO-Suc-Ala-Ala-Pro-Val-chloromethane (ki/Ki = 579 M(-1) S(-1)) occurred via a two-step, irreversible complexing mechanism with potencies one-half and one-fifth that of leukocyte elastase, respectively. Glycosaminoglycans such as chondroitin sulfate, dermatan sulfate and a chondroitin polysulfate, interacted with myeloblastin as non-essential activators in the presence of peptide substrates (activation up to a 6.7-fold factor) and as partial inhibitors (about 50% inhibition at saturation) in the presence of elastin. This property distinguishes myeloblastin from leukocyte elastase, which is always inhibited by glycosaminoglycans, independently of the substrate.

Enzyme Activation↗

PubMed2000

Failure to detect bovine immunodeficiency virus contamination of stud bull spermatozoa, blood leukocytes, or semen leukocytes in samples supplied by artificial insemination centers.

OBJECTIVE: To determine whether bovine immunodeficiency virus (BIV) infection could be detected in spermatozoa, blood leukocytes, or semen leukocytes from stud bulls in artificial insemination centers. ANIMALS: 30 bulls at 3 artificial insemination centers. PROCEDURE: Polymerase chain reaction testing that used 3 sets of primer pairs targeting pol and env regions of the BIV proviral genome was performed on DNA extracted from semen leukocytes, spermatozoa, and blood leukocytes from each bull. Southern blot analysis was performed to increase sensitivity of detection. Western blot analysis of plasma samples was used to detect antibodies against BIV. RESULTS: BIV provirus was not detected in DNA samples obtained from semen leukocytes, spermatozoa, or blood leukocytes, and antibodies against BIV were not detected. CONCLUSIONS AND CLINICAL RELEVANCE: Contrary to our report of high point prevalence of BIV contamination of semen from a single artificial insemination center, bulls of the study reported here did not appear to be infected. Maximum risk of BIV infection in similar bulls was estimated at 10% with a confidence level of 95%.

Animals↗

PubMed1976

Decreased ability of blood leukocytes from patients with tumors of the urinary bladder to act as stimulator cells in mixed leukocyte culture.

Blood leukocytes from patients with active neoplasms of the urinary bladder were found to have a decreased ability to stimulate in one-way mixed leukocyte culture (MLC). The ability of the patients' leukocytes to act as stimulator cells in one-way MLC was assessed by simultaneous comparison to the ability of leukocytes from normal individuals to stimulate. In addition, the ability of the patients' leukocytes to act as responder cells in the one-way MLC was evaluated. Cells from 31 (56%) of 55 patients with active disease exhibited subnormal stimulatory activity in the MLC while 26 of these 31 patients (84%) had normal responsiveness. Cells from 9 of the 55 failed to respond normally. Poor stimulation occurred with both early and advanced disease, and the stimulatory activity increased after tumor removal in 12 of 15 patients who had previously shown subnormal stimulation. Six patients without active disease at the time of testing, in addition to the 55, exhibited normal levels of stimulation and responsiveness. This defective stimulatory activity is suggestive of an acquired, disease-related phenomenon and is not necessarily associated with decreased blood leukocyte responsiveness.

Adult↗

PubMed1991

Function and evolutionary conservation of distinct epitopes on the leukocyte adhesion molecule-1 (TQ-1, Leu-8) that regulate leukocyte migration.

The leukocyte adhesion molecule-1 (LAM-1, TQ=1, Leu-8) in humans, like its murine homologue, MEL-14, is the principal receptor that mediates the binding of leukocytes to high endothelial venules (HEV) of peripheral lymph nodes. In this study, several regions of the protein which mediate receptor function were identified by using a large panel of murine mAb reactive with LAM-1. Individual mAb reacted with LAM-1+ cells with characteristic intensities of immunofluorescence staining, and each bound both lymphocytes and neutrophils. Lymphocyte attachment to HEV was significantly inhibited by the binding of five mAb. In contrast, only two of these mAb were able to completely block the binding of phosphomannan monoester core complex from the yeast Hansenula holstii cell wall (PPME), a phosphomannan monoester core polysaccharide that serves as a soluble model of the natural ligand of LAM-1. Interestingly, the binding of two anti-LAM-1 mAb to cells induced a significant increase in PPME binding, reminiscent of the increase in receptor affinity observed after leukocyte activation. Antibody cross-blocking studies indicated that many of the functionally important epitopes were spatially distinct, and domain mapping indicated that they recognized distinct domains of LAM-1. The expression and function of these epitopes were further assessed by using a variety of animal species to further characterize the functionally relevant epitopes defined in these studies. At least some anti-LAM-1 mAb reacted with leukocytes from monkey, cow, rabbit, sheep, dog, cat, pig, and goat, but not from chicken, rat, or mouse. The reactivity of anti-LAM-1 mAb in several animal species correlated with the ability of leukocytes to bind PPME, and mAb that inhibited lymphocyte binding to HEV in man could also inhibit this function in rhesus monkey and dog. Thus, several LAM-1 epitopes are structurally and functionally well conserved throughout recent mammalian evolution, emphasizing an important role for LAM-1 in the regulation of leukocyte traffic.

Animals↗

PubMed1991

Leukocyte adhesion molecule-1 (LAM-1, L-selectin) interacts with an inducible endothelial cell ligand to support leukocyte adhesion.

The human lymphocyte homing receptor, LAM-1, mediates the adhesion of lymphocytes to specialized high endothelial venules (HEV) of peripheral lymph nodes. We now report that LAM-1 is also a major mediator of leukocyte attachment to activated human endothelium. In a novel adhesion assay, LAM-1 was shown to mediate approximately 50% of the adhesion of both lymphocytes and neutrophils to TNF-activated human umbilical vein endothelial cells at 4 degrees C. The contribution of LAM-1 to leukocyte adhesion was only detectable when the assays were carried out under rotating (nonstatic) conditions, suggesting that LAM-1 is involved in the initial attachment of leukocytes to endothelium. In this assay at 37 degrees C, essentially all lymphocyte attachment to endothelium was mediated by LAM-1, VLA-4/VCAM-1, and the CD11/CD18 complex, whereas neutrophil attachment was mediated by LAM-1, endothelial-leukocyte adhesion molecule-1, and CD11/CD18. Thus, multiple receptors are necessary to promote optimal leukocyte adhesion to endothelium. LAM-1 also appeared to be involved in optimal neutrophil transendothelial migration using a videomicroscopic in vitro transmigration model system. LAM-1-dependent leukocyte adhesion required the induction and surface expression of a neuraminidase-sensitive molecule that was expressed for at least 24 h on activated endothelium. Expression of the LAM-1 ligand by endothelium was optimally induced by LPS and the proinflammatory cytokines TNF-alpha and IL-1 beta, whereas IFN-gamma and IL-4 induced lower levels of expression. The LAM-1 ligand on HEV and cytokine treated endothelium may be similar carbohydrate-containing molecules, because phosphomannan monoester core complex from yeast Hansenula hostii cell wall blocked binding of lymphocytes to both cell types, and identical epitopes on LAM-1-mediated lymphocyte attachment to HEV and activated endothelium. Thus, LAM-1 and its inducible endothelial ligand constitute a new pair of adhesion molecules that may regulate initial leukocyte/endothelial interactions at sites of inflammation.

Antibodies, Monoclonal↗

PubMed1982

Interaction of Borrelia spirochetes with human mononuclear leukocytes causes production of leukocytic pyrogen and thromboplastin.

Relapsing fever caused by Borrelia spirochetes is characterized by episodes of spirochetemia, fever, and DIC. We examined the ability of Borrelia hermsii to induce production of leukocytic pyrogen and thromboplastin from human blood leukocytes in vitro. Organisms were found devoid of endotoxin by the Limulus assay. Human peripheral blood leukocytes were separated into MNC and PMN fractions and were incubated with two to five spirochetes per cell in 10% human serum. Supernatant fluids from MNC-spirochete mixtures produced mean increases in the temperature of rabbits of 0.80 degree to 1.35 degrees C, which were significantly higher than those caused by supernatant fluids of MNC or spirochetes alone (p less than 0.05). MNC-spirochete mixtures possessed seven to 15 times the thromboplastic activity of MNC suspensions alone, assayed with a modified one-stage prothrombin time. Supernatant fluids of PMNs and spirochetes, on the other hand, did not contain leukocytic pyrogen, and PMN suspensions did not produce thromboplastin. Cycloheximide (10 micrograms/ml), and inhibitor of protein synthesis, completely suppressed both pyrogen and thromboplastin production. Although intracellular spirochetes were observed within phagosomes of blood monocytes by electron microscopy, the production of leukocytic pyrogen and thromboplastin was not significantly altered by serum opsonins or by the inhibitors of phagocytosis cytochalasin B (5 micrograms/ml) or phenylbutazone (2 mg/ml). These results showed that Borrelia spirochetes stimulated human MNCs to produce increased amounts of leukocytic pyrogen and thromboplastin and that this stimulation required de novo synthesis of protein, was not mediated by endotoxin, and was not prevented by omitting opsonic proteins or by inhibiting phagocytosis.

Borrelia↗

PubMed1979

Sensitization of leukocytes of cancer patients against fetal antigens: leukocyte migration studies.

Hypertonic extracts from human fetuses (10--22 wk of gestation) were used to test the sensitizaton of leukocytes from cancer patients against fetal antigens in a direct, microcapillary tube assay system. Leukocytes were simultaneously exposed to a panel of allogeneic tumor extracts and a panel of fetal extracts. Leukocytes from 24 gastric cancer patients, 43 colorectal cancer patients, and 13 lung cancer patients were assayed with extracts obtained from gastric, colorectal, and oat cell carcinomas, respectively, and these extracts were also used with leukocytes from 41 patients bearing tumors of various other organs. Significant migration inhibition by tumor extracts was observed in 81.6% of the tests with gastric cancer, 67.4% of the tests with colorectal cancer, 69.0% of the tests with lung cancer, and 51.2% of the tests with other types of cancer. With fetal extracts, significant migration inhibition occurred in 58.3, 58.7, 59.6, and 54.9% of the tests, respectively. Reactivity against fetal extracts did not depend on the gestation age of the fetuses used for extraction. The conclusion was reached that the leukocytes of most of the cancer patients were sensitized against substances contained in fetal extracts irrespective of the type of tumor of the leukocyte donor. The cross-reactivity pattern suggested that 3-M KCl extracts of whole human fetuses contained a complex mixture of specificities related to the various fetal organs and tissues, which may have represented counterparts to most of the tumor-associated specificities.

Antigens↗

PubMed1993

Biocompatibility of leukocyte removal filters during leukocyte filtration of cardiopulmonary bypass perfusate.

To evaluate the biocompatibility and the efficacy of leukocyte removal filters, we performed a prospective study by using the cardiopulmonary bypass perfusate taken from the heart-lung machine for 20 patients who underwent cardiac surgery and were randomly divided into four groups according to the filters used. A leukocyte removal filter was installed in the transfusion line while the perfusate was transfused to the patients. No increases of C3a, C5a, elastase, and thromboxane were found during leukocyte filtration by polyester filters (Optima, Sepacell R500, and Pall RC100). Activation of the complement cascade was observed during filtration by the cellulose acetate filter (Cellselect) although the efficacy of the Cellselect filter was evidently higher than that of the polyester filter. These results imply that polyester leukocyte filters are superior to cellulose acetate filters in terms of biocompatibility but have a reduced efficacy. An optimal leukocyte filter providing both high efficacy and biocompatibility has yet to be developed.

Biocompatible Materials↗