muramidase and Leukopenia

Endotoxemia is considered to be associated with the high mortality of gram-negative septic patients. Increasing evidence shows that beta-lactam antibiotics have a propensity to induce endotoxin release from the bacterial outer membrane while killing bacteria. We have recently found that egg white lysozyme (EW-LZM) shows strong inhibition of beta-lactam induced bacteriolysis and lipopolysaccharide (LPS) release from Escherichia coli O111, resulting in reduction of the LPS-initiated inflammatory response. In this study, we compared the effect of EW-LZM on E. coli J5, which possesses rough-type LPS (RaLPS), in order to demonstrate the effect of O-antigenic polysaccharide on endotoxin neutralizing activity of EW-LZM and on inhibition of beta-lactam induced lysis by LZM. Both of the beta-lactam induced bacterial lysis and subsequent LPS release were almost completely inhibited by EW-LZM. The effect was more potent than that of wild-type LPS as assessed by released LPS concentration and LPS induced cytokine syntheses. In addition, EW-LZM was effective against lethal infection of E. coli J5 in cyclophosphamide induced leukopenic mice. These facts strongly suggested that O-antigenic polysaccharide negatively modulates LPS neutralizing activity of EW-LZM.

Topics: Animals; Anti-Bacterial Agents; Bacteriolysis; Carrageenan; Cell Line; Cyclophosphamide; Disease Models, Animal; Endotoxemia; Endotoxins; Escherichia coli; Escherichia coli Infections; Galactose; Lactams; Leukopenia; Lipopolysaccharides; Macrophages; Male; Mice; Mice, Inbred ICR; Monokines; Muramidase; O Antigens

Course of the disease and some indices of immunity were studied in 100 children with Sonne's and Flexner's dysentery. Parameters of immunity in 32 children (the 1st group) were normal. 68 patients (the 2-nd group) had secondary immune deficiency and leukopenia. Recovery of immunodeficient children in use of antibiotics and prodigiosan was slowed down by 5.2 days as compared to that of children without immunodeficiency. Antibiotics used in combination with lysozyme in patients of the 1st group resulted in restoration of immunological reactivity and recovery in usual terms.

Topics: Acute Disease; Adolescent; Anti-Bacterial Agents; Child; Child, Preschool; Drug Therapy, Combination; Dysentery, Bacillary; Humans; Immunoglobulins; Immunologic Deficiency Syndromes; Infant; Leukopenia; Muramidase; Shigella flexneri; Shigella sonnei; Time Factors

Immunohistological study of 18 cases of histiocytic necrotizing lymphadenitis (HNL) demonstrated numerous helper/inducer cells (OKT-4) and suppressor/cytotoxic cells (OKT-8) with activation (Tac) and proliferation (OKT-9) markers, and histiocytes (lysozyme, alpha-1 anti-chymotrypsin, OK-M1) in the affected areas. However, B cells (B-1), NK cells (Leu-7 and Leu-11), complement proteins and receptor (C4 and C3d receptor), and neutrophils (chloroacetate esterase) were scanty or absent in these foci. Activity of NK cells was also decreased in the peripheral blood of 2 cases examined. The results suggest that HNL might be induced by the abnormal T cell-histiocyte response against some causative agents which induce a similar reaction of delayed hypersensitivity type.

Topics: Adolescent; Adult; Antibodies, Monoclonal; Antigens, Differentiation, T-Lymphocyte; Antigens, Surface; Axilla; Child; Female; Histiocytes; Histocytochemistry; Humans; Immunity, Cellular; Killer Cells, Natural; Leukopenia; Lymphadenitis; Male; Microscopy, Electron; Middle Aged; Muramidase; Neck; Receptors, Complement; Receptors, Complement 3b; T-Lymphocytes

Meningococci and Haemophilus influenzae may invade the subarachnoid space during the bacteriaemic phase without impairment of the blood-CSF barrier and in the absence of any leucocyte reaction. In pneumococcal meningitis the CSF may also contain less than 100 cells/microliter despite the presence of "pure bacterial cultures", but the barrier is completely broken when the serum/CSF concentration ratio is below 10. A clinical analysis of eight patients with fewer than 100 cells/microliter revealed that the first symptoms of meningitis appeared at least 3 days prior to the diagnostic lumbar puncture. There was a strong neutrophilic reaction in the blood with a prevalence of juvenile forms in most cases, indicating intact antibacterial defence mechanisms. Within 24 h after the start of antibiotic therapy the cell number rose above 2000/microliter accompanied by disappearance of pneumococci. Six of the eight patients died. In three cases autopsy revealed thick layers of pus over the convexities, indicating a compartmental separation of the ventricles and the spinal subarachnoid space. In one case of late diagnosed bacterial meningitis with a pleocytosis of 430/microliter the CSF lysozyme level was seven times higher than compatible with this cell number. Hyperphagocytosis and cellular disintegration is thought to cause the leucopenia within the spinal CSF compartment. "Apurulent bacterial meningitis" can be seen as a disease entity that is a diagnostic pitfall and also a prognostic sign.

Topics: Adult; Aged; Bacterial Infections; Blood-Brain Barrier; Female; Glucuronidase; Humans; Leukocyte Count; Leukopenia; Male; Meningitis; Meningitis, Haemophilus; Meningitis, Listeria; Meningitis, Pneumococcal; Middle Aged; Muramidase; Prognosis

Staphylococcal Panton-Valentine leukocidin has been purified and tested in mice for its biological properties. Applied even in high doses the leukocidin was not lethal. It caused however, disturbances in the peripheral blood occurring in several phases. First reaction after leukocidin injection was seen as marked granulocytosis persisting for 16-20 hours and accompanied by lymphopenia. At the same time, decrease in serum lysozyme activity and increase of intracellular digestion by mature granulocytes, was observed. In the second phase, these phenomena have reversed. 131I-labelled leukocidin has been used for the study of distribution of this toxin in the mouse. Accumulation of leukocidin in some tissues was observed. The leukocidin affected not only granulocytes but also other peripheral blood cells.

Topics: Animals; Bone Marrow Cells; Dose-Response Relationship, Drug; Granulocytes; Leukocidins; Leukocyte Count; Leukocytes; Leukocytosis; Leukopenia; Male; Mice; Mitotic Index; Muramidase; Staphylococcus aureus

The effects of an acute Hog Cholera Virus (HCV) infection upon immune functions of experimentally infected pis were studied. Leukopenia was found to occur in both vaccinated and non-vaccinated infected animals but without any decrease in lymphocyte proportion. Lymphocytes from infected pigs had an altered response to phytohemagglutinin (PHA) as judged by an in vitro tritiated thymidine uptake of PHA-stimulated lymphocyte cultures. The beginning of a secondary humoral immune response to lysozyme appeared to be significantly depressed in HCV diseased animals.

Topics: Animals; Antibody Formation; Classical Swine Fever; Classical Swine Fever Virus; Leukopenia; Lymphocyte Activation; Muramidase; Swine; Viral Vaccines

Topics: Animals; Cell Line; Cell Membrane; Endocytosis; Enzymes; Immunoglobulin G; Leukopenia; Liposomes; Lung; Muramidase; Phagocytosis; Pharmaceutical Vehicles; Rabbits

MGI(+)D(+), MGI(+)D(-), and MGI(-)D(-) mouse myeloid leukemic cells, which genetically differ in their competence to be induced to undergo normal cell differentiation in vitro by the normal macrophage- and granulocyte-inducing protein MGI, were analyzed for their ability to undergo cell differentiation in diffusion chambers in vivo. As after induction by MGI in vitro, MGI(+)D(+) clones were induced for Fc and C3 rosettes, lysozyme, and mature macrophages and granulocytes in normal syngeneic or allogeneic mice. MGI(+)D(-) clones were also induced in these mice for all these properties, although in vitro they were not induced by MGI for mature cells. The MGI(-)D(-) clones were induced in vivo for C3 and Fc rosettes, lysozyme, and intermediate stages but not for mature cells, whereas none of these properties were induced in these clones by MGI in vitro. Thus, certain types of myeloid leukemic cells differentiate better in vivo, possibly due to the presence of higher effective concentrations of MGI and/or other inducing factors, and MGI(+)D(+) and MGI(+)D(-) cells can completely differentiate in vivo to mature cells. In vivo differentiation was inhibited in mice treated with cyclophosphamide. It was also inhibited in various strains of nude mice, except for one MGI(+)D(+) clone, where it was inhibited in C57BL/6 but not in ICR nude mice. This MGI(+)D(+) clone was also the only clone that was induced to differentiate normally in vitro by a 23,000 molecular weight form of purified MGI. The results suggest that different clones respond to different molecular forms of MGI, which may be present in different proportions in some animals, that in vivo differentiation by MGI possibly with other factors may be regulated by cells involved in the immune response, and that this differentiation can be genetically controlled. Differentiation in vivo was enhanced by injection of conditioned medium containing MGI and by inoculation of MGI-producing cells, including normal granulocytes. This indicates that the induction of normal differentiation of myeloid leukemic cells in vivo can be enhanced by these treatments.

Topics: Animals; Bone Marrow Cells; Cell Differentiation; Colony-Stimulating Factors; Cyclophosphamide; Granulocytes; Leukemia, Myeloid; Leukopenia; Macrophages; Mice; Mice, Inbred C57BL; Mice, Inbred ICR; Mice, Nude; Muramidase; Neoplasms, Experimental; Phenotype; Species Specificity

A spontaneous oscillation of the white blood cell count was observed in a 58 year old man with chronic myelogenous leukemia (CML). Similar cyclic variations were noted in the platelet and reticulocyte counts with no apparent alterations in marrow cellularity to account for such changes. Since direct correlation was noted between white blood cells, platelets, and reticulocyte counts versus spleen size, it suggests that splenic hemopoiesis may be responsible for these cyclic changes. A possible inverse relationship between colony-stimulating factor (CSF) activity and the white blood cell count was noted, suggesting that CSF may be the humoral agent controlling granulocyte production. A direct correlation between the white blood cell count and serum unsaturated vitamin B12 binding capacity (UBBC) and lysozyme was also noted and further supports the concept that the latter two are measures of the granulocyte pool and metabolism. An inverse relationship between CSF activity and the UBBC suggests that these may be two different entities. Finally a modified form of standard chemotherapy may be effective in inducing remission in cases of CML with marked cyclic leukocytosis-leukopenia.

Topics: Alkaline Phosphatase; Blood Cell Count; Blood Platelets; Bone Marrow Examination; Colony-Stimulating Factors; Erythropoietin; Hemoglobins; Humans; Karyotyping; Leukemia, Myeloid; Leukocyte Count; Leukocytosis; Leukopenia; Male; Middle Aged; Muramidase; Periodicity; Reticulocytes; Spleen; Vitamin B 12

Topics: Aged; Anemia; Chronic Disease; Female; Hepatomegaly; Humans; Leukemia, Myeloid; Leukopenia; Muramidase; Reticulocytes; Splenomegaly

Topics: Animals; Chronic Disease; Dogs; Gingivitis; Leukopenia; Mechlorethamine; Muramidase

Topics: Adolescent; Adult; Bone Marrow; Bone Marrow Cells; Diagnosis, Differential; Humans; Leukopenia; Middle Aged; Muramidase

Topics: Agranulocytosis; Immune Sera; Leukocytes; Leukopenia; Mechlorethamine; Muramidase; Time Factors

Topics: Antibodies; Carbon Isotopes; Endotoxins; Glycolysis; Humans; In Vitro Techniques; Leukocytes; Leukopenia; Muramidase; Phosphotransferases; RNA; Tritium; Uridine

Topics: Animals; Eosinophils; Leukocyte Count; Leukopenia; Muramidase; Rats

Topics: Adult; Aged; Female; Humans; Leukopenia; Male; Middle Aged; Muramidase; Neoplasms; Radiation Effects; Radiation Injuries; Radiation-Protective Agents; Radioisotope Teletherapy

Topics: Antimitotic Agents; Antineoplastic Agents; Humans; Leukocyte Disorders; Leukopenia; Muramidase; Toxicology

Topics: Antineoplastic Agents; Cyclophosphamide; Cytostatic Agents; Female; Humans; Leukopenia; Muramidase; Toxicology; Triaziquone; Uterine Cervical Neoplasms

Topics: Antineoplastic Agents; Antiviral Agents; Humans; Iatrogenic Disease; Leukocyte Disorders; Leukopenia; Muramidase; Neoplasms; Radiation-Protective Agents; Toxicology

Topics: Ascorbic Acid; Cyclophosphamide; Leadership; Leukocyte Disorders; Leukopenia; Muramidase; Neoplasms; Propionates; Radiation-Protective Agents; Testosterone; Toxicology