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J Biewenga

Publications and source records attributed to J Biewenga.

At least 37 records · Page 2Linked to original sources

Electronmicroscopic examination of white cell reduction by four white cell-reduction filters.

The mechanisms of white cell (WBC) reduction in 16-hour-old CPDA-1 red cell (RBC) concentrates by filtration on a column filter and on three different flatbed filters were studied by electron microscopy, with special emphasis on cell-to-cell interaction, cell damage, and interaction of blood cells with the material. Generally, lymphocytes were removed by mechanical sieving and monocytes by adherence and mechanical sieving. Granulocyte depletion occurred by mechanical sieving, direct adhesion to the fibers, and indirect adhesion to activated and spread platelets. In the column filter, most granulocytes were captured by adhesion. In the coarse layers of two of the flatbed filters, indirect adhesion was most prominent, whereas direct adhesion was most prominent in the other flatbed filter. For the most part, granulocytes were captured by direct adhesion in the fine layers, but in one flatbed filter, capture apparently occurred by mechanical sieving. The results of this study suggest that the efficiency and the mechanism of WBC reduction depend on the physicochemical characteristics of the non-woven materials in the filters as well as the cellular composition of the RBC concentrates.

Blood Transfusion↗

Comparison of five different filters for the removal of leukocytes from red cell concentrates.

The leukocyte depletion capacity and performance of 5 filters designed for filtration of red cell concentrates (RCC) were compared by counting leukocytes, measuring red cell volumes and by histological examination of the filters after use. To eliminate interdonor differences, 5 buffy-coat-poor RCC were pooled (in each of 10 experiments) and subsequently split up into the original bags. The RCC were passed over the Cellselect filter, a column filled with cellulose acetate, and over flat-bed polyester filters: the Cellselect Optima, the Pall RC 50, the Leukostop and the Sepacell R-500. The filtration was shortest with the Pall RC 50 (p less than 0.001 compared to the other 4 filters). Leukocyte removal was most effective with the cellulose acetate filter (p less than 0.01 compared to the other 4 filters) followed by the Cellselect Optima polyester filter (p less than 0.02 compared to the remaining 3 filters). Residual leukocytes did not exceed 50 x 10(6) for any brand of filter. Red cell recovery was similar for all 5 filters with mean values from 86.1 to 89.2%. The leukocyte numbers, counted in Türk's solution or in propidium iodide, gave comparable values in hemocytometers applying light microscopy or fluorescent microscopy, respectively. Histological examination showed that lymphocytes were mainly removed by trapping, whereas granulocytes showed a variable pattern: adhesion in presence of platelets or trapping.

Blood Component Removal↗

Lymphocytes and nonlymphoid cells in human nasal polyps.

Immunohistochemical stainings were performed on polyp specimens of 48 patients and on mucosal biopsy specimens of the middle and inferior turbinates of 23 and 28 patients, respectively. Significantly more CD8+ (suppressor/cytotoxic) than CD4+ (helper/inducer) cells were found in the polyps. The number of CD2+, CD4+, and CD8+ lymphocytes in nasal polyps were very similar to the number in the macroscopically unaffected mucosa of the middle turbinates, whereas scores in the inferior turbinates were lower. In healthy subjects, the differences were smaller. CD22+ B cells were detected in varying numbers in the polyps in more or less organized clusters. Significantly more HLA-DR+ cells were found in polyps and middle turbinates than in the inferior turbinates. Eosinophils were found in moderate to large numbers in polyps of 77% of the patients. Mast cells and plasma cells were detected in moderate numbers, whereas neutrophils were found in 35% of the patients. In the middle and inferior turbinates varying but small numbers of eosinophils, mast cells, plasma cells, and neutrophils were found. In considering these findings, the role of chronic inflammation with T cell-dependent disturbances is discussed with regard to the pathogenesis of nasal polyps.

Adolescent↗

Immunoglobulin concentrations in nasal secretions differ between patients with an IgE-mediated rhinopathy and a non-IgE-mediated rhinopathy.

Nasal secretions from patients with an IgE-mediated rhinopathy, patients with a non-IgE-mediated rhinopathy, and healthy control subjects were collected with a newly developed direct aspiration system. Total protein, albumin, secretory IgA (sIgA), IgE, IgG, and IgM concentrations were measured in the nasal secretions to detect whether the nasal pathology is reflected in nasal secretion protein concentrations. It was found that protein and immunoglobulin concentrations in nasal secretions were inversely related to amount of secretion in the nasal cavity. Both patients' groups had a significantly higher sIgA to protein ratio than the healthy control subjects. Furthermore, patients with an IgE-mediated rhinopathy had significantly higher sIgA and IgM to total protein ratios in their nasal secretions than patients with a non-IgE-mediated rhinopathy. Probably these differences are due to changes in immunoregulation.

Adolescent↗

The in situ immune response of the rat after intraperitoneal depletion of macrophages by liposome-encapsulated dichloromethylene diphosphonate.

This study concerns the contribution of peritoneal macrophages in vivo to local and systemic immune responses in the rat. Peritoneal macrophages as well as macrophages in the draining parathymic lymph nodes were selectively eliminated by intraperitoneal inoculation of dichloromethylene-diphosphonate-containing liposomes. This depletion resulted in an enhanced immune reaction to intraperitoneally administered trinitrophenyl keyhole limpet haemocyanin in the parathymic lymph nodes, as demonstrated by the higher numbers of specific anti-TNP antibody-forming cells in macrophage-depleted animals than in control animals from day 5 after immunization. The immune reaction peaked at day 7 and remained high until day 10. Specific antibody-forming cells were found occasionally in the mesenteric lymph nodes and spleen, but not in the mucosa of the gut or in the bronchus-associated lymphoid tissue. An elevated immune reaction found in parathymic lymph nodes associated with the depletion of local macrophages by liposome treatment indicates a regulatory role of peritoneal macrophages in local humoral immune response.

Animals↗

Mucosal and systemic antibody formation in the rat after intranasal administration of three different antigens.

In order to study the role of nasal-associated lymphoid tissue (NALT) in the local nasal immune response, rats were immunized intra-nasally with either of the following trinitrophenylated (TNP) antigens; the thymus-dependent keyhole limpet haemocyanin (KLH), or the thymus-independent lipopolysaccharide (LPS), or with the particulate (thymus-dependent) sheep red blood cells (SRBC). Primary responses hardly occurred, while only TNP-KLH elicited a considerable secondary response. The major responding organ was the posterior cervical lymph node. Specific antibody-forming cells (AFC) occurred in the medulla and were mainly of the IgA or IgG isotype. Hardly any specific AFC were found in NALT or the surrounding mucosa. Intranasal immunization evoked no antibody response in the lung. Ample anti-TNP antibodies could be detected in the sera of animals, primed and boosted with TNP-KLH or TNP-LPS. No specific serum antibodies occurred after immunization with TNP-SRBC. The results are discussed in view of the immunological defence in the upper respiratory tract.

Administration, Intranasal↗

Histologic and immunohistochemical studies on the preparation of white cell-poor red cell concentrates: the filtration process using three different polyester filters.

Three third-generation white cell (WBC)-depletion filters based on polyester layers with decreasing pore size were investigated. In the coarse layers, unaggregated granulocytes, monocytes, and platelets and aggregates of these cells were captured in close contact with the fibers. This indicates that the depletion of granulocytes, monocytes, and platelets in the coarse layers of the filters is due in part to activation and adhesion with the formation of cell clusters on the fibers. In Filter I and Filter II platelets were not found in the fine layers, whereas in Filter III, 70 percent of the platelets were detected as unaggregated platelets on the fibers of the fine layers. More than 95 percent of the lymphocytes captured in the three filters occurred as single cells in the fine layers, and over 60 percent of these could be recovered. This suggests that the depletion of lymphocytes depended on trapping of the cells in the fiber network. All three filters captured HLA-DR-positive lymphocytes in the top layers, a finding that supports earlier reports that the transfusion of filtered red cell concentrates reduces HLA alloimmunization. More lymphocytes and granulocytes were found in the last layer of Filters II and III than of Filter I. Therefore, the risk of white cell leakage is probably lowest for Filter I. Red cells were found as red cell aggregates in the fine layers of Filters I and II, whereas almost no red cells were detected in Filter III. It was shown that the three filters studied were similar in their removal of WBCs, but differed in their mechanisms of removal.

Blood Platelets↗

Nasal secretions from patients with polyps and healthy individuals, collected with a new aspiration system: evaluation of total protein and immunoglobulin concentrations.

This study was designed, first, to test a new system for aspiration of human nasal secretions and, secondly, to evaluate protein and immunoglobulin concentrations in these secretions at different levels of secretory activity. The direct aspiration system combines the advantages of minimal irritation of the nasal mucosa with the facility to determine concentrations per gram of secretion. The total protein and immunoglobulin concentrations were inversely related to the amount of secretion obtained. Variations in fluid secretion throughout the day may be responsible for this relationship. The inverse relationship was much more significant in patients with nasal polyps, in which much higher concentrations were found, than in healthy subjects. Ratios of immunoglobulin to total protein were independent of the amount of secretion obtained. Compared to the controls, the ratios of IgM and IgG to protein in the secretions of the patients were significantly increased. The secretory immunoglobulin A to total protein ratios were only slightly higher in the patients' secretions.

Adolescent↗

Lymphoid and non-lymphoid cells in nasal-associated lymphoid tissue (NALT) in the rat. An immuno- and enzyme-histochemical study.

Lymphocyte and macrophage subpopulations and the stroma of mucosa-associated lymphoid tissue in the nasal cavity of the rat were examined by application of immunohistochemical and enzyme histochemical methods to cryostat sections. Nasal-associated lymphoid tissue was composed of a loose reticular network with lymphocytes and macrophages, covered by epithelium. The epithelium was infiltrated with B cells. T helper (W3/13-positive) and T suppressor/cytotoxic or large granular cells (OX8-positive), ED1-positive macrophages and Ia-positive cells. The B cell areas were populated by B cells, immunopositive for surface IgM or IgG. B cells with surface IgA or IgE were rare. Germinal centres were found infrequently. T helper cells were scattered throughout the B cell area. A few ED1-positive macrophages and ED5-positive follicular dendritic cells were observed. Strong Ia staining (mostly of B cells) was found in this area. The T cell areas contained T helper and T suppressor/cytotoxic cells in about equal amounts, and numerous ED1-positive macrophages. ED1 staining was also found in the subepithelial area. Numerous ED1-, ED2- and ED3-positive macrophages were found in the border between the lymphoid mass and the surrounding connective tissue. A few non-lymphoid cells showed weak acid phosphatase or non-specific esterase activity. The morphological observations suggest that nasal-associated lymphoid tissue plays an important role in the first contact with inhaled antigens.

Animals↗

The localization of macrophage subsets and dendritic cells in the gastrointestinal tract of the mouse with special reference to the presence of high endothelial venules. An immuno- and enzyme-histochemical study.

This study concerns the distribution of macrophages and dendritic cells (DC) in the gastrointestinal tract of the mouse. Heterogeneity of macrophage population was found by using the MOMA-1, MOMA-2, ERTR-9, Mac-1 and F4/80 monoclonal antibodies. MOMA-1, ERTR-9, Mac-1 and F4/80+ cells were detected mostly at the villous cores in the lamina propria of the villi, whereas MOMA-2+ cells were primarily found around the crypts at the base of the villi. These MOMA-2+ cells revealed a granular appearance throughout the cytoplasm and displayed a strong acid phosphatase (AcPh) activity. Few MOMA-2+ cells were seen at the top of the villi in the epithelium. Although MOMA-1 and ERTR-9+ cells have similar morphology and the same distribution patterns in the lamina propria, they are likely different populations, because in Peyer's patches (PP), MOMA-1+ cells were present, whereas ERTR-9+ cells could not be detected. Both populations displayed AcPh activity. Strongly stained Mac-1+ cells were abundantly seen in the lamina propria of the small intestine. F4/80+ cells were rare. NLDC-145+ cells with AcPh activity and weak Ia staining were also found. In the PP-associated villi and in the T-dependent area of PP, dendritic NLDC-145+ cells, which were strongly Ia positive, were detected. MIDC-8+ cells were found only in the T-dependent area. Few NLDC-145+ cells (dendritic cells) were found in the upper part of the oesophagus. These cells were also stained with the MIDC-8 antibody.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The effects of Peyer's patches inactivation in the rat on the development of antibody-forming cells to intestinal antigen.

The effects of Peyer's patch (PP) inactivation on local and systemic immune response in rats was investigated. A cauterization method has been developed to inactivate PP. Animals were primed intraperitoneally or intragastrically with trinitrophenyl-keyhole limpet haemocyanin (TNP-KLH) one day before cauterization, and were challenged intraintestinally two weeks later. The secondary immune response in the spleen, mesenteric lymph node (MLN) and intestinal villi was studied by immunohistochemistry. Histological observations on PP after inactivation showed that most T cells in the interfollicular area had disappeared, as had B cells in the follicle. T cells repopulated PP much slower than B cells. Complete recovery of PP occurred no earlier than 2 weeks after inactivation. The immunization experiments revealed higher numbers of anti-TNP antibody-forming cells (anti-TNP AFC) of IgM, IgG and IgA isotypes in the spleen of the PP-inactivated animals than in the controls. Very few anti-TNP AFC were found locally in the lamina propria of the intestinal villi or in the MLN in both groups. It is suggested that PP play a role in the regulation of systemic immune responses against intestinally-administered thymus-dependent antigen. Moreover, inactivation of PP could alter the antigen uptake by gut epithelium and the local antigen processing. As a result, an increased amount of antigen could reach the spleen eliciting a higher immune response.

Animals↗

Histological and immunohistochemical studies on the preparation of leukocyte-poor red cell concentrates by filtration: the filtration process on cellulose acetate fibers.

A histological and immunohistochemical investigation of slices from the Cellselect leukocyte filter showed that the capture of lymphocytes within these filters depended on trapping of the cells in the cellulose acetate fiber network more than on adherence. Probably, additional mechanisms played a role in granulocyte removal. Microaggregates of granulocytes and platelets were found at the top of the Cellselect leukocyte filter. Therefore, it is likely that granulocyte and platelet removal, at least in part, is due to the formation of cell clusters on the surface of the fibers. Although a part of the original, nonfiltered, leukocytes already showed morphologic characteristics of cell necrosis, more necrotic leukocytes were detected within the filter.

Blood Cells↗

An immunohistochemical study on the postnatal development of rat nasal-associated lymphoid tissue (NALT).

This study concerns the development of nasal-associated lymphoid tissue in the rat, using immuno- and enzyme-histochemical staining techniques on cryostat sections. Nasal-associated lymphoid tissue is present at birth as a small accumulation of mainly T lymphocytes and nonlymphoid cells; B cells are rare. Distinct areas of T and B cells appear at 10 days after birth; by that time high endothelial venules are also observed. Intra-epithelial lymphocytes are present, most of them being T-helper cells. ED1+ macrophages are seen throughout the tissue. The proportion of ED1+ cells does not change during ontogeny. ED2+ cells (tissue macrophages) are present predominantly at the border between the lymphoid tissue and the surrounding connective tissue, in all age-groups. ED3+ mononuclear cells are scattered throughout the nasal-associated lymphoid tissue of young animals. Later on, the ED3+ cells migrate into the border-area between lymphoid and connective tissue. Ia+ non-lymphoid cells in the nasal lymphoid tissue increase in number during ontogeny. Only a few of them show acid phosphatase activity, indicating that the proportion of classical scavenger macrophages is low. Some of them may be antigen presenting (dendritic) cells. Ia+ dendritic cells also occur between the epithelial cells. Moreover, some epithelial cells express the Ia marker.

Aging↗

Lymphocytes and nonlymphoid cells in the nasal mucosa of patients with nasal polyps and of healthy subjects.

Immunohistochemical stainings were performed on biopsy specimens of the middle and inferior turbinates of the nasal mucosa of 14 patients with nasal polyps and 16 healthy subjects. Significantly more CD8+ (T suppressor/cytotoxic) cells than CD4+ (T helper/inducer) cells were found in the lamina propria of the middle and inferior turbinates of patients with nasal polyps and in the inferior turbinate of healthy subjects. The middle and inferior turbinates of healthy subjects contained significantly more CD4+ cells than the middle and inferior turbinates of patients with nasal polyps. CD19+ B cells were hardly detected in the patients and healthy subjects. More HLA-DR+ cells were found in the middle than in the inferior turbinate, especially in the patients. Varying but small numbers of eosinophils, neutrophils, mast cells, and plasma cells were found in patients and healthy subjects. The possible role of CD4+, CD8+, and HLA-DR+ cells in the nasal mucosa is discussed with regard to the pathogenesis of nasal polyps.

Adolescent↗

Binding of human IgA1 and IgA1 fragments to jacalin.

Interaction of jacalin, an N-terminal galactose specific lectin, with human IgA1 and IgA1 fragments was investigated. IgA1 and all galactose containing fragments bound to jacalin-Sepharose, including Fab fragments containing only the galNac linked to serine-224 and Fc fragments containing four gal-galNac sequences. These data indicate that both the galNac and gal-galNac sequences can interact with jacalin. Jacalin precipitated IgA1 and the fragments F(abc)2, F(ab')2 and Fc in agar gel and from solutions. It also precipitated Fab' fragments in agar gel. Jacalin did not precipitate Fab fragments significantly. This suggests that, except for the single binding site on the Fab fragments containing the galNac linked to serine-224, jacalin itself also has a limited number of sites to interact with N-terminal galactose residues. ELISA studies revealed that intact IgA1 had a lower jacalin binding capacity than F(abc)2 fragments which lack CH3 domains, than F(ab')2 which lack the CH2 and CH3 domains, and than Fc fragments containing four gal-galNac sequences. This led to the conclusion that part of the galNac or gal-galNac sequences in intact IgA1 molecules are inaccessible to interaction with jacalin. Cleaving the C-terminal domains off may have induced a reorientation of the hinge region structure, including the orientation of the carbohydrate units.

Animals↗

Intra-epithelial lymphocytes and non-lymphoid cells in the human nasal mucosa.

Immunohistochemical staining of biopsy specimens was used to investigate the occurrence of lymphocyte subsets and non-lymphoid cells within the epithelial layer of the human nasal mucosa. The CD19 (B cell) marker was not expressed on the intra-epithelial lymphocytes, whereas the pan T cell marker CD2 was varyingly detected. The HLA-Dr antigen was abundantly present on epithelial cells, lymphocytes, and non-lymphoid cells. The latter are probably dendritic or Langerhans' cells. The findings stated above were the same in patient and control samples. In biopsy sections of 9 ear, nose, and throat patients, many CD8-positive (T suppressor/cytotoxic) cells and very few weakly stained CD4-expressing (T helper/inducer) cells were present. Quantification on single-cell preparations showed an average of 67% of the lymphocytes to be CD2 positive, 73% to be CD8 positive, while only 12% of the lymphocytes expressed the CD4 antigen. In control sections CD8 was similarly present as in patient sections, and, in addition, some clearly stained CD4-positive cells were seen.

Adolescent↗

Effect of serum albumin on the recovery of human IgA1 from immobilized jacalin.

Published methods for affinity purification of human IgA1 on immobilized jacalin are based on binding through galNac residues in the IgA1 hinge region. The present study shows that in addition to this galNac-dependent binding an 'alternative' binding mechanism, involving protein-protein interactions, is operative. Moreover, human (HSA) and bovine (BSA) serum albumins were also observed to interact with jacalin through the 'alternative' mechanism, though much more weakly than IgA1. HSA and BSA did not interfere with the galNac-dependent binding of IgA1, but inhibited the 'alternative' binding of IgA1 to jacalin-Sepharose, probably by competition. Thus, IgA1 from serum samples was almost completely bound through the galNac-dependent mechanism, but part of the IgA1 from samples containing little or no HSA or BSA was bound by the 'alternative' mechanism. Washing of jacalin-Sepharose columns with excess BSA could disrupt the 'alternative' binding and subsequent washing with 0.8 M D-galactose in 0.5 M NaCl/PBS was sufficient to elute all IgA1. The 'alternative' binding to jacalin is probably not restricted to the above-mentioned proteins. Purification of IgA1 by precipitation with jacalin and subsequent gel filtration of the D-galactose-dissolved precipitate was not practical, since jacalin-IgA1 precipitates did not dissolve completely and new complexes were formed during the gel filtration procedure.

Binding Sites, Antibody↗

Activation of complement by human serum IgA, secretory IgA and IgA1 fragments.

UNLABELLED: Activation of the complement (C) system by human IgA was studied. Both subclasses of IgA, IgA1 and IgA2, and secretory IgA were shown to activate C, as determined by deposition of C3 on glutaraldehyde-activated microwells coated with IgA. The activation of the C system occurred in the presence of MgEGTA and not in D-deficient serum. In addition to C3, deposition of properdin (P) but not of C4 was detected. These results indicate that C activation, as determined by measuring deposition of C3 and P, occurred by the alternative pathway (AP). The data further show that the major part of the hinge region, which is deleted in IgA2 as compared with IgA1 and which forms the major structural difference between the two subclasses, is not involved in C activation. Reduction and alkylation destroyed the ability of IgA to activate C, as has also been demonstrated for IgG. In order to define the C activating region of the IgA molecule, several fragments of IgA1 were tested. The four-chain molecules F(ab')2 and F(abc)2 were shown to activate the AP. No activation was observed with the two-chain fragments Fab and Fc. The Fc fragment of IgA also did not activate the CP, as does the Fc fragment of IgG. This indicates that activation of the AP of C by IgA is dependent on the presence of the F(ab')2 fragment. IN CONCLUSION: human IgA does activate C by the AP. This activation requires an intact F(ab')2 fragment.

Complement Activation↗