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PubMed1975

The isolation and partial characterization of neutrophil chemotactic factors from Escherichia coli.

Heat-stable, chemotactically active peptides have been obtained from Escherichia coli culture filtrates. They range in size between 150 and 1500 daltons and are anionic at neutral pH. Free carboxyl groups but not free amino groups appear to be required for activity. The N-terminal group may be blocked. There do not appear to be internal aromatic or basic residues in the chemotactically active fractions. A highly purified, not completely characterized, fraction was found to contain aspartic acid, serine, glutamic acid, alanine, and glycine.

Acetylation↗
PubMed1992

Complement, neutrophil, and macrophage activation in women with severe preeclampsia and the syndrome of hemolysis, elevated liver enzymes, and low platelet count.

Activation of complement, neutrophils, and macrophages was studied in 14 women with severe preeclampsia, 11 of whom had the syndrome of hemolysis, elevated liver enzymes, and low platelet count; in 14 women with normal pregnancies; in seven normal pregnant women undergoing cesarean deliveries; and in 15 healthy nonpregnant women. Activation of complement, neutrophils, and macrophages was measured by plasma determinations of complement split products, polymorphonuclear (PMN) elastase, and neopterin, respectively. Women with severe preeclampsia had increased levels of C5a, terminal complement complex, PMN elastase, and neopterin at delivery and 1 day postpartum as compared with the normal pregnant group. One week postpartum, neopterin remained higher in preeclamptic women, whereas the complement components and PMN elastase had returned to normal. Cesarean delivery after normal pregnancy did not increase the levels of complement split products, PMN elastase (except for one value), or neopterin. The nonpregnant women had normal PMN elastase and neopterin levels. Accordingly, complement, neutrophils, and macrophages are activated in women with severe preeclampsia at delivery. The plasma levels of PMN elastase correlated positively to the formed terminal complement complexes in vivo. An in vitro study was performed to elucidate further the connection between complement and leukocyte activation. Recombinant C5a incubated in whole blood and in a neutrophil cell suspension gave a dose-dependent release of PMN elastase. Both the clinical and the in vitro results indicate that activation of the complement system may affect the function of neutrophils. This study supports the theory that the pathologic manifestations of severe preeclampsia may be explained by complement-induced release of biologically active substances from activated leukocytes.

Biopterins↗
PubMed1975

[Present problems of somatic cell genetics].

A review of recent advances in genetics of somatic cells is given in the article. It contains three sections: 1) hybridization of somatic cells and its application to the mapping of genes and to the study of gene action; 2) relation of somatic cell genetics to genetic engineerings; 3) progress and perspectives of higher plant somatic cell genetics.

Animals↗
PubMed1991

Neutrophil kinetics in the pulmonary microcirculation during acute inflammation.

The site of neutrophil interaction with the vasculature during acute lung inflammation is controversial, but has been suggested to occur in the alveolar capillaries, in contrast with its location in postcapillary venules in nonpulmonary tissues. We studied the kinetics of neutrophil accumulation and the site of neutrophil-vascular interaction in the lung by examining directly the behavior of fluorescein isothiocyanate-labeled canine neutrophils utilizing in vivo fluorescence videomicroscopy through a window inserted into the chest wall of anesthetized dogs. The administration of fragments of the fifth component of complement (C5f) into either the airway or pulmonary artery resulted in neutrophil sequestration almost exclusively in pulmonary capillaries. Kinetically, there was a shift in the distribution of neutrophil transit times resulting in a marked prolongation of median transit time. This response occurred within seconds after intravascular C5f and within 5 minutes after airway C5f and was maintained for at least 30 minutes. Ultrastructural studies after airway C5f showed neutrophils in various stages of migration through the alveolar-capillary membrane and more than 90% of these neutrophils were seen to migrate from capillary rather than from venular sites. These data indicate that pulmonary inflammation differs from inflammation in other vascular beds primarily in the site of neutrophil localization and migration. This fundamental difference in the inflammatory response may serve to localize the inflammatory response to the alveolus, and (since cells were retained singly), indicates the inability of leukoaggregation adequately to explain the findings. Leukocyte accumulation in the lung may thus occur through alterations in the balance between delivery of neutrophils to the lung and the transit time of these cells across the capillary bed.

Acute Disease↗
PubMed1977

Stimulated neutrophil locomotion: chemokinesis and chemotaxis.

All leukocytes are capable of responding chemotactically (oriented locomotion) and chemokinetically (stimulated nondirected or random locomotion) to a variety of chemical agents. A brief review of the in vitro and in vivo methods of studying neutrophil movement and our present knowledge of chemotactic factors is presented as well as a discussion on the mechanisms of stimulated movement. Two clinically important instances of defects in neutrophil movement, ie, the Chédiak-Higashi syndrome and a case of actin dysfunction, are herein described.

Ascorbic Acid↗
PubMed1978

Intracellular control of human neutrophil secretion. I. C5a-induced stimulus-specific desensitization and the effects of cytochalasin B.

Human neutrophils released the granule constituents myeloperoxidase and lysozyme, but not the cytoplasmic enzyme lactic dehydrogenase, when pretreated with cytochalasin B and stimulated with purified human C5a. Prior exposure to C5a before the cytochalasin B, however, abrogated the subsequent secretory process. Interaction of neutrophils with C5a was shown to result in a concentration-dependent rapid desensitization that could not be overcome by later addition of cytochalasin B or of cytochalasin B and C5a. The effect was relatively stimulus specific in that neutrophils desensitized in this manner could be induced to release granule enzymes by casein or by complement-coated zymosan particles. Cytochalasin B effects on neutrophils appear to mimic those of surface binding of soluble stimuli such as C5a and immune complexes. It is suggested that desensitization in concert with surface stimulation may represent an important intracellular mechanism for limiting neutrophil secretion.

Caseins↗
PubMed1985

[Cellular and humoral bases of allergic reactions].

The inflammatory symptoms of allergic reactions are caused by complex interactions of mediator substances. They are either split from humoral precursor molecules by proteolytic enzymes or released from various cells. Mediators may cause the allergic symptoms directly or act on other mediators and mediator systems. New activities may be generated by mediator cooperation. Mediator systems can be activated by immunological antigen-specific and nonimmunological nonspecific mechanisms. In a given reaction both types of induction mechanisms are involved. It is not possible to relate a certain allergic symptom to a certain mediator or a set of mediators.

Anaphylaxis↗
PubMed1989

In vivo studies of antibody dependent acantholysis.

The data that are being accumulated on the mechanisms by which pemphigus autoantibodies induce acantholysis in vivo conform that tissue injury in pemphigus is a complex phenomenon where several effector mechanisms may interact. Active research is being performed in many laboratories around the world, employing both in vitro and now in vivo models to further define this unique autoimmune disease.

Acantholysis↗
PubMed1988

Plasma levels of main granulocyte components during cardiopulmonary bypass.

Plasma levels of granulocyte lactoferrin, myeloperoxidase, and elastase in alpha 1-proteinase inhibitor complex were compared with C3a and C5a levels in 10 patients undergoing cardiopulmonary bypass. At the end of the operation, plasma levels of lactoferrin increased from 97.0 +/- 22.8 to 1257 +/- 139.8 ng/ml, myeloperoxidase increased from 37.1 +/- 4.3 to 170.9 +/- 34.9 ng/ml, and elastase in alpha-proteinase inhibitor complex rose from 89.4 +/- 7.4 to 437.8 +/- 97.3 ng/ml. There was also a significant anaphylatoxin formation. To investigate the relationship between complement and granulocyte activation, patients undergoing cardiopulmonary bypass received the calcium channel blocker nifedipine (orally and intravenously) and the antiplatelet drug dipyridamole. The continuous infusion of nifedipine (5.91 +/- 0.53 micrograms/kg body weight per hour) caused significantly lower levels of elastase in alpha-proteinase inhibitor complex and lactoferrin but not anaphylatoxin. Dipyridamole was without effect on complement and granulocyte activation during cardiopulmonary bypass. Our data demonstrate inhibition of granulocyte activation during cardiopulmonary bypass by continuous infusion of nifedipine, even in the presence of complement activation.

Aged↗
PubMed1987

Drug activity "in vitro" and "in vivo" on leucocyte chemotaxis.

Drug influences on polymorphonuclear leucocytes (PMN) and particularly on PMN migration was investigated. PMN chemotaxis and random migration were assessed in vitro, after drug incubation in vitro and/or administration in vivo. An inhibiting effect on directed migration induced both by fMLP and C5a was demonstrated with some anti-inflammatory drugs whereas random migration was unaffected. The effect was dose-related and linked to drug chemical structure and to physiopathological state of the cells. Similar results may be obtained after administration in vivo. However some examples show that metabolism can inactivate the pharmacological effect of chemical substances and that the route of administration is of prime importance. The activity of new pathological compounds on PMN migration might need to be studied both in vitro and in vivo. In vitro experiments might be performed as a first step of the study. However only in vivo experiments are really representative of potential therapeutical use. Thus we conclude that both experimental series may be performed to appreciate drug interaction with PMN functions during clinical assays.

Animals↗
PubMed1988

Tumor necrosis factor enhances susceptibility of vascular endothelial cells to neutrophil-mediated killing.

Tumor necrosis factor has a variety of effects on different types of cells in vitro, including endothelial cells. The current studies show that pretreatment of rat pulmonary artery endothelial cells with tumor necrosis factor increases in a time- and dose-dependent manner their sensitivity to killing by neutrophils stimulated with phorbol myristate acetate or C5a. Similar effects are seen with interleukin-1. These data suggest that tumor necrosis factor and interleukin-1 may have important pro-inflammatory effects on endothelial cells.

Animals↗