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Biomedical subjects

W Pruzanski

Publications and source records attributed to W Pruzanski.

At least 127 records · Page 7Linked to original sources
PubMed1983

Lymphocytotoxic and phagocytotoxic activity in progressive systemic sclerosis.

Sera of 66 patients with progressive systemic sclerosis (PSS) were tested for cold and warm reacting lymphocytotoxins (LCT). Cold LCT were found in 30 (45%) patients, 18 of whom also had warm LCT. Warm LCT alone were found in 14 patients. Twenty-nine sera with cold LCT were tested and reacted with both peripheral B and T lymphocytes. There was predominant killing of B cells in 52% and of T cells in 14%. Ten cold LCT were absorbed to and eluted from peripheral blood lymphocytes. All eluates were cytotoxic to B and T cells; 1 killed predominantly T cells and 2 killed predominantly B cells. Clinical-laboratory and HLA correlations with cold LCT showed no significant differences between the LCT-positive group and the LCT-negative group. Granulocytotoxins were rare in PSS, but warm reacting monocytotoxins were found in 33 cases (57%). Crossreactivity of cytotoxins was tested using eluates from various cells. The majority of eluates from lymphocytes were cytotoxic against polymorphonuclears (PMN) and monocytes. Some eluates from PMN and from monocytes had lymphocytotoxic activity. This suggests existence of common antigenic determinants on various cells against which cytotoxins are directed.

Antibodies↗
PubMed1983

The influence of lysostaphin on phagocytosis, intracellular bactericidal activity, and chemotaxis of human polymorphonuclear cells.

Lysostaphin, a microbicidal enzyme that lyses Staphylococcus aureus, was introduced to study phagocytosis and ICBA (Tan et al.3) on the presumption that it does not penetrate into the phagocytic cells. It was recently suggested, however, that LS enters the cells and kills ingested bacteria. By using two methods to study phagocytosis and bactericidal activity, the old one based on disruption of PMNs and plating technique and a new one that does not require disruption, we found that LS did not influence phagocytosis or phagocytic index but altered intracellular kill of Staphylococcus. LS eliminated almost completely extracellular bacteria, but centrifugation and washing of PMN at the end of phagocytic assay were almost equally efficient. Since the method of disruption of PMN and plating of bacteria cannot distinguish penetration of LS to the cells from its adherence to the outer wall of PMN, we employed a new, recently described acridine orange/crystal violet method, which can measure simultaneously phagocytosis and ICBA and eliminates completely extracellular microorganisms. This method has shown that in the presence of LS, a significantly higher proportion of staphylococci were killed intracellularly--91% +/- 2.7 vs. 74% +/- 2.9 (p less than 0.001), i.e., that LS either penetrated to the cells or enhanced ICBA. It was also found that trypsin, which was used as an inhibitor of LS, was unable to abolish bactericidal activity of LS. It is suggested that LS should not be used for assessment of ICBA but may be employed for studies of phagocytosis over short incubation periods. A new method based on acridine orange/crystal violet staining was found to be useful for investigation of phagocytosis and ICBA of human PMNs.

Blood Bactericidal Activity↗
PubMed1983

Modulation of phagocytosis and bactericidal activity of human polymorphonuclear and mononuclear phagocytes by antiarthritic agents.

The influence of 9 antiarthritic drugs on phagocytosis and intracellular bactericidal activity of human polymorphonuclear (PMN) and mononuclear phagocytes was investigated using gram-positive and -negative microorganisms and latex particles. With the exception of prednisone all the other agents suppressed phagocytosis and/or phagocytic index of PMN. Whereas naproxyn suppressed phagocytosis of all 3 particles used, other drugs had more pronounced inhibitory activity on phagocytosis of E. coli than of S. aureus or latex particles. Monocytes were less influenced by antiarthritic agents. Intracellular bactericidal activity was markedly suppressed by phenylbutazone, oxyphenbutazone, naproxyn and gold sodium thiomalate. In suboptimal conditions when serum was omitted from the assay, dual action of some drugs was observed. It may be concluded that antiarthritic agents may modulate phagocytosis and intracellular bactericidal activity. The modulation was most pronounced in conditions similar to those in vivo i.e., with added serum and when the cells were exposed to antiarthritic agents for longer time. It should be taken into consideration while assessing defense mechanisms and susceptibility to infection in rheumatic diseases.

Anti-Inflammatory Agents↗
PubMed1982

Functional characterization of the cells in chronic neutrophilic leukemia.

Light and electron microscopy of neutrophils from chronic neutrophilic leukemia (CNL) did not reveal differences from normal mature neutrophils. However, functional characterization of CNL cells showed marked differences when compared to normal cells. CNL neutrophils were much less viable in suboptimal conditions. Their survival was further reduced by autologous serum and was corrected by normal human serm. CNL cells showed very active phagocytosis, but their bactericidal activity was reduced in suboptimal conditions. The total content of lysozyme and beta-glucuronidase was lower in CNL cells compared to normal neutrophils, but the release of these enzymes from stimulated cells was much higher than normal. This observation is compatible with a marked lysosomal lability. Cells from the patients' peripheral blood and bone marrow showed excessive growth in CFU-C assays. Marked susceptibility of CNL cells to cytotoxic activity of cold agglutinins, SLE sera, and CSFs was observed and may signify qualitative and/or quantitative differences in the membrane structure of CNL neutrophils, as compared to normal cells.

Aged↗
PubMed1982

Circulating immune complexes in patients with progressive systemic sclerosis.

Forty-one patients with progressive systemic sclerosis were studied for the presence of immune complexes by the fluid- and solid-phase C1q binding, C1 activation, and the fluid-phase conglutinin assays. Complement activation and autoantibodies were also studied. Immune complexes were detected in only 6 patients (15%); activation of complement was found in 5 others. The clinical and serologic features of patients with complexes were compared with those in whom complexes were not identified. No significant difference was found with respect to serology. Organ involvement was generally more frequent in the group with immune complexes, but the difference was statistically significant only with respect to lung involvement. The present data suggest that, although complement-fixing immune complexes are infrequently detected in progressive systemic sclerosis, they may play a role in the pathogenesis of lung lesions associated with the disease.

Adult↗
PubMed1982

B-cell neoplasms with homogeneous cold-reacting antibodies (cold agglutinins).

Among 78 patients with persistent cold agglutinins, 31 had lymphoma, 13 had macroglobulinemia of Waldenstrom, six had chronic lymphocytic leukemia and 28 had chronic cold agglutinin disease. The average age was over 60 years. Patients wit chronic cold agglutinin disease had more hemolytic crises, bleeding and Raynaud's phenomena, and less frequently lymphadenopathy or hepatosplenomegaly. The frequency of anemia, positive Coombs test results, cryoglobulinemia and Bence Jones proteinuria was similar in the various groups. Survival time from diagnosis was on average two years in lymphoma, two and a half years in Waldenstrom's macroglobulinemia, more than six years in chronic lymphocytic leukemia and more than five years in chronic cold agglutinin disease. Anti-I were common in chronic cold agglutinin disease (74 percent) and rare in other groups (32 to 33 percent). Anti-I and other cold agglutinins were rare in chronic cold agglutinin disease and common in lymphoma and Waldenstrom's macroglobulinemia. In chronic cold agglutinin disease, and in Waldenstrom's macroglobulinemia, cold agglutinins usually had K light chains--92 percent and 71 percent, respectively--whereas in lymphoma, 71 percent of cold agglutinins had lambda light chains. The type of light chains related to the specifically of cold agglutinins: 58 percent of IgM/K were anti-I, 75 percent of IgM/lambda had other specificities. Cold agglutinins were cytotoxic to autologous and allogeneic cells were killed implying that the former may be precoated in vivo with the antibodies. In conclusion, conditions with persistent cold agglutinins are a spectrum that varies from "benign" autoimmune-like chronic cold agglutinin disease to malignant lymphoma. Marked differences in the light chain type of cold agglutinins, specificity toward membranous antigens and severity of clinical manifestations were noted in benign and malignant varieties.

Adult↗
PubMed1982

Reactivity of cold agglutinins with subsets of human lymphocytes of various origins.

Forty-five cold agglutinins (CA) were tested against various populations of lymphocytes by cytotoxicity and immunofluorescence assays. Marked differences were observed between anti-I and anti-i CA. Thirty-six per cent of anti-I killed preferentially peripheral blood and tonsillary B lymphocytes, whereas only 12 per cent killed preferentially T lymphocytes. Anti-I killed a much higher proportion of B-chronic lymphocytic leukemia cells than peripheral blood lymphocytes, peripheral blood B cells or T-chronic lymphocytic leukemia cells. Forty-three per cent of anti-i killed preferentially peripheral blood T lymphocytes and 54 per cent killed preferentially tonsillary T cells, whereas only 14 per cent killed more peripheral blood B cells and none killed preferentially tonsillary B cells. The kill of thymic lymphocytes and T-chronic lymphocytic leukemia cells by anti-i was very high, whereas the kill of B-chronic lymphocytic leukemia cells was very low. Almost all CA of other than I-i specificities showed preferential kill of peripheral blood B (83 per cent) and tonsillary B (67 per cent) cells. Tonsillary lymphocytes were usually more susceptible to the cytotoxic activity of CA than peripheral blood lymphocytes. Cold agglutinins with kappa light chains killed more B cells whereas CA with gamma light chains seemed to kill more T cells. Cytotoxicity did not correlate to the utilization of complement. It is suggested that the density and/or the accessibility of membranous antigens may be different on B and T cells, or alternatively that in addition to antigens common to all lymphocytes, anti-I and non-I/i cold agglutinins recognize specific antigenic determinants on B lymphocytes, whereas anti-i cold agglutinins recognize specific antigenic determinants on T lymphocytes.

Agglutinins↗
PubMed1981

New antigenic determinant (Sa) on human lymphocytes and phagocytes.

Presence of antigenic determinants reacting with homogeneous IgM/kappa cold agglutinin (CA) of a new specificity, tentatively called Sa, was investigated by bithermic cytotoxicity assay and by immunofluorescence. CA Sa killed on average 38% allogeneic peripheral blood lymphocytes (PBL) and up to 74% of autologous PBL. There was preferential kill of B-PBL compared to T-PBL. Some preference toward B cells was also noted using tonsillary B and T lymphocytes. Cytotoxic activity of CA Sa against chronic lymphocytic leukemia cells of B-type was almost equal to that of potent anti-I CA and much stronger than anti-i CA. Presence of additional B-cytotoxic factor in the serum was excluded by the use of red blood cell eluate composed solely of homogeneous CA. Thymocytes and helper-type T cells from a patient with T cell chronic lymphocytic leukemia were very susceptible to the cytotoxic action of Sa. CA Sa killed 39% of monocytes, but there was almost no kill of polymorphonuclear leukocytes. Lymphocytotoxicity of CA Sa was abolished by sialyllactose and was not influenced by I-active glycoproteins. Comparison of CA Sa to CA of other specificities showed marked differences, supporting the view that Sa has new, previously unrecognized specificity.

Aged↗
PubMed1981

Intrahepatic cholestasis with predominant pericentral deposition in systemic amyloidosis.

Liver involvement in amyloidosis is rarely associated with intrahepatic cholestasis. The cases recorded in the literature indicate that there is a tendency toward periportal deposition, leading to centrilobular cholestasis. Our case was most interesting in that the amyloid deposition was most severe in the centrilobular area. Presumably there was still sufficient compression of canaliculi at the periportal level to produce obstruction of the bile flow. This would appear to be a less common but distinct variant of systemic amyloidosis with associated obstructive jaundice.

Amyloidosis↗
PubMed1981

Multiple myeloma with discordant M components in the serum and CSF.

A patient with multiple myeloma was initially seen with Bence Jones-type kappa proteinemia and intermittent Bence Jones proteinuria. In the late stage of the disease, involvement of the CNS was observed, and abnormal plasma cells were found in the CSF. Chromosomal analysis of these plasma cells showed an accessory chromosome in the A2 group and an abnormal chromosome in the D13 group. In addition to Bence Jones-type kappa protein similar to that in the serum, the CSF contained IgA-kappa M component. Immunoquantitation detected 250 mg/dL of IgA in the CSF and only 33 mg/dL in the serum. T our knowledge, such discordance of M components has never been described before.

Bence Jones Protein↗
PubMed1980

Plasma cell neoplasia with peripheral polyneuropathy. A study of five cases and a review of the literature.

Peripheral polyneuropathy (PPN) is a rare complication of plasma cell neoplasia (PCN), occurring in less than one percent of the patients. Fifty-four such patients (including our 5) were reviewed. There were 42 men (78%) and 12 women (22%) aged 28 to 72 years. Forty-nine percent of patients were younger than 51 years at the time of diagnosis. The initial complaints were different from those observed in multiple myeloma in general, and were related to polyneuropathy in 80% of the patients. PPN was usually of a mixed sensory-motor type and most often involved all four extremities. Skeletal pain was less common than in myeloma in general, occurring initially in 15% and at diagnosis in 45% of the patients. In 21 patients, reversibility of neuropathy was observed. These patients were compared to those with irreversible neuropathy and found to be relatively younger and more aggressively treated with irradiation and modern chemotherapy. Elevated sedimentation rate was uncommon. Less than half of the patients had anemia, and six patients, all with osteosclerotic lesions, had polycythemia. Azotemia was detected in 44% of the cases. No hypercalcemia was observed in 21 examined patients. M components were usually of IgG class, and when the light chains of M components were examined they were invariably of lambda type. Often the level of M component was below 2.0 g/dl. In all patients the bone marrow was infiltrated with immature, abnormal-looking plasma cells, but the infiltrate was often limited to one or a few foci. Solitary plasmacytoma was observed in 14 patients. No anemia, hypercalcemia or azotemia was recorded in this group. Eight patients had serum M components. Bone marrow aspirate was usually normal. In seven patients definite reversibility of PPN was observed after irradiation of plasmacytoma. Twelve patients presented with osteosclerotic lesions (22%), 18 with both osteosclerotic and osteolytic lesions (33%) and 13 with osteolytic lesions. Forty-two percent of the patients had less than three visible lesions in the skeleton. Eleven patients had either osteoporosis or radiologically normal skeleton. The mean survival from the first symptom was about 28 months and from the diagnosis 20 months. The five-year survival was 21% and 20%, respectively. These observations highlight the differences between PCN with PPN and multiple myeloma without PPN.

Adult↗
PubMed1980

A new human monoclonal cold agglutinin Sa recognizing terminal N-acetylneuraminyl groups on the cell surface.

A human homogeneous IgM/K cold agglutinin (CA) Sa is described, whose corresponding antigen on erythrocytes (RBC) was abolished by neuraminidase. This indicated that the antigen was related to N-acetylneuraminic acid, similar to Pr and Gd antigens. In contrast, this antigen was only partially destroyed by proteases, whereas Pr antigens are completely destroyed and Gd antigens are not influenced by proteases. Sa antibody activity was inhibited by sialyllactose NeuAc (alpha 2 leads to 3) (alpha 2 leads to 6) Gal (beta, 1 leads to 4) Glc like anti-Gd but in contrast to anti-Pr. The corresponding antigen was associated with an RBC membrane glycoprotein fraction like Pr, Sa is one of a spectrum of human monoclonal CA against cell surface neuraminyl groups.

Aged↗
PubMed1980

Lymphadenopathy associated with dysgammaglobulinemia.

Conditions in which lymphadenopathy is associated with dysgammaglobulinemia may be divided into two groups: those in which etiologic factors and pathogenesis are well established, and those which are still a medical dilemma. Only a few belong to the former group: infections, immunizations, and drug-induced conditions being the best examples. Unfortunately, the great majority belong to the latter group. Interestingly enough, many conditions with lymphadenopathy and dysgammaglobulinemia share similar histologic features, such as infiltration with lymphocytes, immunoblasts, plasma cells, and histiocytes. This pleomorphic infiltration may appear together with prominent vascular proliferation. In animal experiments, angiogenesis was induced by administration of immunocompetent lymphocytes into the skin of unimmunized, irradiated mice. Therefore such lymphocyte-induced angiogenesis may be a manifestation of the graft-versus-host reaction. Recent developments in immunology, such as the discovery of many membranous markers and receptors on the lymphocyte membrane, the study of cytoplasmic structure and synthetic products, detection of enzymatic aberrations and chromosomal abnormalities, and refinement in histochemical techniques, have led to attempt to reclassify lymphoplasmacytic and leukemic disorders. Indeed, several classifications coming from different coutries and from various centers in the same country have been proposed, leading to a typical "Tower of Babel" phenomenon. It is obvious that more knowledge of etiologic factors and pathogenetic mechanisms is necessary to classify, cure, and eventually prevent the diseases described in this paper.

Adolescent↗