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At least 19 recordsLinked to original sources
PubMed1985

Opposing effects of dexamethasone on the clonal growth of granulocyte and macrophage progenitor cells and on the phagocytic capability of mononuclear phagocytes at different stages of differentiation.

Dexamethasone, a synthetic glucocorticosteroid, was shown to modulate the colony-stimulating factor-dependent clonal growth of myeloid progenitor cells in semisolid agar cultures, enhancing the formation of granulocyte colonies (50-100%) and suppressing the formation of macrophage colonies (75-97%). Modulation of the pattern of myeloid colony formation by dexamethasone (12-125 nM) was brought about when the steroid was administered to 6-day cultures at the time of culture initiation and up to 72 hr later. Dexamethasone inhibited myeloid cell proliferation when administered to 5-day liquid cultures at culture initiation and up to 96 hr later. Dexamethasone (12-250 nM) also enhanced the phagocytic activity of bone marrow-derived mononuclear phagocytes toward heat-killed (HK) yeast cells (up to 100%) and IgG-coated sheep red blood cells (up to 60%). Enhancement of the phagocytic capability depended critically on the stage in culture at which dexamethasone was administered. Exposure to dexamethasone for 28 hr up to 96 hr of 96-hr cultures of bone marrow cells did not lead to a modulation of phagocytic activity of the developing mononuclear phagocytes. The presence of dexamethasone during the critical period of 96 hr to 120 hr after culture initiation led to an enhanced phagocytic capability, which was statistically significant already 12 hr after the administration of the glucocorticoid. Dexamethasone induced an enhanced phagocytic activity when administered at any time after culture initiation provided that it was in culture during this critical period. When added at 120 hr of culture, dexamethasone no longer enhanced the phagocytic capability of mononuclear phagocytes and when added later than 156 hr of culture suppressed it. Dexamethasone also suppressed (up to 68%) the phagocytic capability of resident and elicited peritoneal macrophages. The results suggest that glucocorticoids shift the balance of granulocyte vs. macrophage formation at early stages of precursor cell differentiation. Reduction in mononuclear phagocyte growth and enhancement of its phagocytic capability might reflect accelerated differentiation/maturation steps. The inhibitory effect of dexamethasone on macrophage formation and on the phagocytic capability of mature mononuclear phagocytes and peritoneal macrophages might be a relevant aspect of the in vivo immune suppression encountered after glucocorticoid administration.

Animals↗
PubMed2001

In vitro effect of temperature on phagocytic and cytotoxic activities of splenic phagocytes of the wall lizard, Hemidactylus flaviviridis.

The in vitro effect of temperature on phagocytosis, nitric oxide production and interleukin-1 (IL-1) secretion by splenic phagocytes isolated from the wall lizard (Hemidactylus flaviviridis) demonstrated that changes in temperature altered non-specific defenses. The LPS-induced percentage phagocytosis and phagocytic index were recorded maximum at 25 degrees C. The phagocytic activity declined considerably when the phagocytes were incubated at low (7 and 15 degrees C) or high (37 degrees C) temperatures. The presence of bacterial lipopolysaccharide (LPS) in the incubation medium could considerably enhance the phagocytic activity of splenic phagocytes. A similar temperature-related effect was also observed on LPS-induced cytotoxic activity of phagocytes. LPS could stimulate the nitrite release indicating nitric oxide production only at 25 degrees C. Likewise, the proliferative responses of immature rat's thymocytes to LPS-induced phagocyte-conditioned medium suggest that IL-1 secretion was enhanced when phagocytes were cultured at 25 degrees C. This suggests that 25 degrees C is the optimal temperature for phagocyte functions in H. flaviviridis. The decrease or increase in temperature other than at 25 degrees C dramatically suppressed the phagocyte activities.

Animals↗
PubMed1978

Attack of sea urchin eggs by dogfish phagocytes: model of phagocyte-mediated cellular cytotoxicity.

To test whether lysosomal degranulation of phagocytes is associated with antibody-dependent cytotoxicity, eggs of Arbacia punctulata were used as targets for blood phagocytes of Mustelus canis. Eggs were coated with heat-aggregated dogfish IgM and exposed to phagocytes, and cytolysis of eggs was observed by Nomarski optics. Phagocytes adhered, degranulated, and raised fertilization membranes resembling those induced by sperm or ionophore A23187. Lysis was then observed as damage radiating from the point of phagocyte-egg contact. By 4 hr, coated eggs exposed to phagocytes released 8.9, 12.3, and 7.4% of total catalase (EC 1.11.1.6), beta-glucuronidase (EC 3.2.1.31), and superoxide dismutase (EC 1.15.1.1) into the medium. Cytotoxic enzyme release significantly exceeded that from uncoated eggs incubated with phagocytes or eggs alone (uncoated or coated). Because activated eggs release a neutral protease, it was considered possible that this enzyme might be responsible for autolysis of eggs. This possibility was excluded because (i) lysis of eggs was not inhibited by soybean trypsin inhibitor (SBTI) whereas the egg protease was sensitive to SBTI, and (ii) the major trypsin-like activity of phagocytes was not inhibited by SBTI. These experiments demonstrate that Ig-coated cells are first activated, and then killed, when exposed to degranulating phagocytes and suggest that enzymes from attacking phagocytes, and not target cells, are responsible for cell death.

Animals↗
PubMed1976

Age-dependent resistance of chickens to salmonella in vitro: phagocytic and bactericidal activities of splenic phagocytes.

The phagocytic and bactericidal activities to Salmonella pullorum (strain 9-25) or Salmonella senftenberg (strain 99D) were examined in chicken splenic phagocytes from 0-day-old to 2-month-old chickens. The phagocytic activity against S pullorum increased in splenic phagocytes from chickens older than 7 days, but significant changes in activity against S senftenberg were not observed during the experimental period. The bactericidal activity of splenic phagocytes against S senftenberg was higher than that of phagocytes against S pullorum during the same period. Increase of the bactericidal activity against S pullorum was observed with increasing age, but the activity of the splenic phagocytes from 0-day-old chickens against S senftenberg was similar to that of the phagocytes from 2-month-old chickens. Although delayed hypersensitivity was confirmed by delayed wattle reaction in 2-month-old chickens sensitized with living S pullorum, the sensitization did not markedly affect phagocytic and bactericidal activities.

Age Factors↗
PubMedDate not supplied

Effects of electrolytic bilateral symmetric lesions of the arcuate nucleus on the phagocytic activity and on the phagocytic response in rats.

Previous researches of Cluj-Napoca laboratories of Physiology (Benetato, Baciu et al., 1945, 1946, 1947) demonstrated that direct electrical stimulation of the tubero-mammillary area in dogs increases, in the following hours, the blood polymorphonuclears phagocytic activity. By contrast, electrical damage of the same region produces a depression of the basal phagocytic activity and a blocking of the phagocytic response (Baciu et al., 1958, 1988). In the present research we assumed there is a stimulating effect of the arcuate nucleus, located in this area, on the phagocytic activity of blood neutrophils. We used an anodal current to stereotaxically induce lesion of the arcuate nucleus in six rats. A control group of six animals was used. Five days later, phagocytic response was induced with a Gram negative bacterial extract given i.v. The results demonstrated a decrease of the phagocytic activity from 164.31 +/- 17 bacteria engulfed by 100 neutrophils in controls, to 138 +/- 12.8 in the lesioned group p < 0.05. Phagocytic response after five hours appears depressed in the lesioned group (138 +/- 12.8 to 156.25 +/- 13.3, p < 0.05). Similar results were obtained after 24 hours. In control animals the response is very significant after 5 and 24 hrs., respectively, (p < 0.001). In conclusion, the arcuate nucleus is moderately involved in sustaining the basal phagocytic activity of blood neutrophils. It has an important role in phagocytic response.

Adjuvants, Immunologic↗
PubMedDate not supplied

Effects of monosodium glutamate on blood neutrophils phagocytic activity and phagocytic response in mice.

Previous researches of our laboratories (1945, 1946, 1947) have shown that direct electrical stimulation of the tubero-mammillary hypothalamic area in dogs enhances the blood neutrophils phagocytic activity and the phagocytosis exhibiting leukocytes percent. After electrolytic damage of the same area, phagocytic activity decreases and phagocytic response is suppressed (1985, 1988). In the present work, we performed in mice extensive chemical lesions of the arcuate nucleus, by means of the neonatal treatment with monosodium glutamate (MSG). The experiment was carried out on 23 new-born mice. 15 mice were injected with MSG (G group), the other 8, serving as control group, received isotonic saline solution (C group). The studied parameters were, in both groups, the weight evolution of the animals, the blood neutrophils and lymphocytes percentual variation and the neutrophils' phagocytic activity, tested in vitro, expressed through the number of bacteria engulfed by 100 neutrophils and through the phagocyting neutrophils percentage. Phagocytic activity was tested in whole heparinised blood, against E. coli. Phagocytic response was elicited by i.p. injecting 0.05 ml bacterial suspension and was tested four hours later. The results show that the arcuate nucleus has little influence upon maintaining basal phagocytic activity--that does not significantly decrease after its chemical damage--, but plays a decisive role in triggering the phagocytic response. The neonatal MSG treatment also determines a decrease of the blood lymphocytes percentage and induces obesity in up to 30 days old mice pups.

Animals↗
PubMed1992

Phagocyte metabolic activity during hemodialysis with different dialyzers not affecting the number of circulating phagocytes.

Overall leukocyte counts decrease during certain forms of hemodialysis, but little information is available on the intradialytic evolution of phagocytic metabolic function, especially during dialysis with dialyzers not affecting the number of circulating phagocytes. This study evaluated the phagocytic capacity of granulocytes and monocytes to generate CO2 out of glucose under basic unchallenged conditions and after stimulation with latex or zymosan, before and after 15, 60 and 240 minutes of dialysis with reused cuprophan, AN69S, polysulphone, polymethylmethacrylate and hemophan hemodialyzers. Phagocytic metabolic function was assessed in whole blood on the basis of 14CO2-production from labelled glucose during the phagocytic process. There were no changes in basic unchallenged CO2-production with any of the dialyzers. Reactivity to latex and zymosan, expressed per number of phagocytes, showed no decrease, irrespective of the membrane type. For polymethylmethacrylate and reused cuprophan, a slight but significant increase in metabolic reactivity was observed in response to latex and zymosan. The test employed may give a screening picture of the phagocytic reaction to contact with dialyzers and membranes and thus of their degree of biocompatibility towards the phagocyte system.

Biocompatible Materials↗
PubMed1999

A phagocytic challenge with IgG-coated erythrocytes depresses macrophage respiratory burst and phagocytic function by different mechanisms.

A phagocytic challenge with IgG-coated erythrocytes (EIgG) previously has been shown to cause impaired macrophage respiratory burst capacity and FcgammaR-mediated phagocytic function. Because both the respiratory burst and FcgammaR-mediated phagocytosis are dependent on the release of arachidonate (AA), we evaluated the effects of impaired AA release on the depression of macrophage function caused by a phagocytic challenge. Challenge with EIgG caused a depression of A23187-stimulated AA release that was associated with impaired phorbol myristate acetate (PMA)-stimulated H2O2 production and FcgammaR-mediated phagocytic function. In contrast, challenge with IgG-coated glass beads (BIgG) had no effect on either AA release or H2O2 production but did depress phagocytic function. Exogenous AA prevented the depression of H2O2 production but had no effect on phagocytic function. Phospholipase A2 (PLA2) activity was depressed under conditions where AA release was impaired. The depression of phagocytic function was correlated with a depression of both EIgG binding and FcgammaR expression. Thus, a phagocytic challenge with EIgG results in macrophage dysfunction by depressing PLA2 activity and depleting FcgammaR.

Animals↗
PubMed1995

Effect of anaesthetic agents on the phagocytic function of human polymorphonuclear leukocytes through analysis with a phagocytic plaque method.

We examined the effects of the intravenous anaesthetic agents, thiamylal and ketamine, on the phagocytic function of polymorphonuclear leukocytes (PMN) in heparinized peripheral blood from healthy individuals using the phagocytic plaque method. Subclinical doses of thiamylal caused enhancement of the phagocytic activity of PMN and super-clinical doses of thiamylal inhibited phagocytic activity of PMN. Ketamine did not adversely affect phagocytic function at relevant therapeutic concentrations. The results presented in this manuscript indicate the phagocytic plaque method can provide a quantitative assessment of the phagocytic function of leukocytes. This method may prove useful in determining whether anaesthetic agents and other drugs adversely affect leukocyte function and hence help prevent the increased susceptibility to infection which can occur in anaesthetized patients. Conversely, the phagocytic plaque method may prove useful in the search for immune-enhancing drugs.

Adult↗
PubMedDate not supplied

Effects of thymectomy on blood neutrophils phagocytic activity and phagocytic response in mice.

The role of the thymus in maintenance of the basal phagocytosis of blood neutrophils and eliciting the phagocytic response, induced by i.v. Escherichia coli, was studied in 9 NMRI thymectomized and in 12 control mice. Thymectomy depresses the percentage of phagocyting neutrophils from 70.91 +/- 0.9 (mean +/- SEM) in controls, to 61.49 +/- 2.33 in the thymectomized rats. Phagocytic activity, as assessed by the number of bacteria engulfed by 100 neutrophils, was also lower in thymectomized mice (114.42 +/- 7.52) than in controls (163.71 +/- 4.53). A phagocytic response to i.v. Escherichia coli could nevertheless be noted in thymectomized mice, their phagocytic activity rising from the basal activity of 114.42 +/- 7.52 to 142.19 +/- 5.40 three hours after injection of Escherichia coli, while in control animals this activity rose from 163.71 +/- 4.53 to 216.46 +/- 12.91. These results may, at least partially, explain the recurrent infections and the septicemia occurring in children with Down's syndrome. It is suggested that the thymus, as an endocrine organ, may be involved in maintaining the basal phagocytic activity of blood neutrophils, while the phagocytic response is modulated by extrathymic mechanisms.

Animals↗
PubMed1993

Cytokine cross-talk between phagocytic cells and lymphocytes: relevance for differentiation/activation of phagocytic cells and regulation of adaptive immunity.

Cytokines represent one of the most important elements in the communication among different cell types. They play an increasingly better understood role in the communication among hematopoietic cells and in particular in the reciprocal regulation of effector cell types of innate or natural resistance (phagocytic cells and Natural Killer (NK) cells) and those of adaptive immunity (T and B lymphocytes). Lymphocytes produce several cytokines with either stimulatory (e.g., colony stimulatory factor) or suppressive (e.g., tumor necrosis factors and interferons) effects on proliferation of early hematopoietic cells. Many of these cytokines, alone or acting in synergistic combinations, also have a differentiation-inducing ability on immature myeloid cells and act as powerful potentiators of the cellular functions of terminally differentiated phagocytic cells. The communication between lymphocytes and phagocytic cells is not unidirectional, as phagocytic cells produce factors that regulate lymphocyte activation. In addition to their role as antigen presenting cells expressing costimulatory accessory molecules and secreting cytokines (e.g., IL-1, IL-6, TNF), phagocytic cells have been recently shown to produce Natural Killer cell Stimulatory Factor (NKSF/IL-12). IL-12 is a heterodimeric cytokine with important modulatory functions on cytotoxicity of NK and T cells, lymphocyte proliferation, lymphokine production, and development of T helper cell subsets. These communications between phagocytic cells and lymphocytes are further regulated by negative and positive feedback mechanisms that contribute to maintain the homeostasis of the system in physiologic conditions and to govern the changes in this equilibrium needed for the response to infectious or other foreign agents.

Animals↗
PubMed2004

Apocynin inhibits NADPH oxidase in phagocytes but stimulates ROS production in non-phagocytic cells.

Apocynin is a naturally occurring methoxy-substituted catechol, experimentally used as an inhibitor of NADPH oxidase. Since it acts as a potent inhibitor in studies with neutrophils and macrophages, no inhibitory effect can often be found in non-phagocyte cells. In our experiments, apocynin even stimulated reactive oxygen species (ROS) production by vascular fibroblasts. Even when added to macrophages, apocynin initially caused an increase in ROS production. The inhibition of ROS formation followed, suggesting that in the presence of leukocyte myeloperoxidase and hydrogen peroxide, apocynin is converted to another compound. Apocynin pre-activated with H2O2 and horseradish peroxidase (HRP) inhibited ROS production immediately. In non-phagocytes, apocynin stimulated ROS production and no inhibition was observed even after 60 min. Apocynin treated with H2O2 and HRP, however, decreased ROS production in the same manner as in macrophages. The stimulatory effect on ROS production can be abolished by tiron and superoxide dismutase (SOD), suggesting that superoxide was the produced species. The effect of apocynin was inhibited by diphenylene iodinium (DPI), a non-scavenging NADPH oxidase inhibitor. It can be summarized that apocynin stimulates cell superoxide production. In the presence of peroxidase and hydrogen peroxide, however, it is converted into another compound that acts as an inhibitor of superoxide production. It strongly suggests that under conditions in vivo, apocynin can have opposite effects on phagocytes and non-phagocyte cells. It acts as an inhibitor of phagocyte NADPH oxidase but also as a ROS production stimulator in non-phagocyte cells.

Acetophenones↗
PubMed2000

Luminescence studies of the phagocyte response to endotoxin infusion into normal human subjects: multiple discriminant analysis of luminescence response and correlation with phagocyte morphologic changes and release of elastase.

A blood luminescence system (BLS) was employed to analyze blood phagocyte function in response to infusion of endotoxin (4 ng Escherichia coli lipopolysaccharide (LPS)/kg body weight) into 7 healthy human subjects. The subjects were closely monitored clinically, and extensive chemical, hematological and coagulation measurements were taken during the pretreatment, early (symptomatic, 1-8 h post-LPS), and late (asymptomatic, 12-48 h post-LPS) phases of acute inflammation. BLS assessment included measurement of basal and PMA-stimulated phagocyte oxidase and myeloperoxidase (MPO) activities, and also included measurement of circulating (COR) and PAF-primed maximum (MOR) opsonin receptor-dependent phagocytic activities. Basal oxidase activity peaked at T + 1 h and showed an additional peak at T + 24 h post-LPS. The COR activity also peaked at 1-2 h, but remained elevated through T + 24 h post-LPS, while the basal MPO activity peaked only once at T + 1 h. We concluded that while MPO evidence of phagocyte respiratory activation returned to baseline by T + 4 h, COR evidence of receptor expression (receptor alert) remained elevated through T + 24 h. During this early (0-8 h) period, elastase/alpha 1AT complex concentration peaked at T + 3-4 h and again at T + 8 h. Peak numbers of circulating polarized and vacuolated phagocytes also appeared at T + 3 h and 7 h. We concluded that there was biochemical and morphological evidence of continuing phagocyte activity beyond T + 4 h to T + 8 h, and that this corresponded with the period during which the subjects were symptomatic. In addition, the appearance of a second peak of basal oxidase activity at T + 24 h, multiple discriminant analyses of all the luminescence data, and the sustained elevation of lactate suggested that there was a later second stage (T + 12 h to 48 h) of the human response to endotoxin, during which time the subjects were asymptomatic.

Adult↗
PubMed1995

Increased phagocytic capacity of the blood, but decreased phagocytic activity per individual circulating neutrophil after an ultradistance run.

The effect of a long strenuous endurance exercise on the phagocytic function of neutrophils was examined. 9 athletes [7 males, 2 females, age: 36-68 years, body mass: 64 (SD 10) kg, height: 175 (SD 10) cm] completed a competetive 100 km run in 8:07 (median value; range: 7:29-9:50 hours). In a whole blood assay the phagocytosis of opsonized E. coli, the receptor density of the Fc gamma receptor 3 (CD16) and the complement receptor 3 (CD11b, direct immunofluorescence) of neutrophils were measured on a per cell basis by flow cytometry before and up to 3 hours after the race. The phagocytic rate (percentage of neutrophils incorporating bacteria) was unchanged after exercise, whereas the phagocytic activity (number of incorporated bacteria per cell) was significantly reduced by -34 (SD 8) % (Wilcoxon test, P < 0.001). The total phagocytic capacity of the blood increased 2-3fold post exercise. The surface antigen expressions of CD11b and CD16 were unaffected by the ultradistance run. The results indicate either a reduced phagocytic function of neutrophils on a single cell basis or the mobilization of neutrophils of the marginal pool with a lower phagocytic activity. However, after a long endurance exercise the phagocytotic capacity of the blood was enhanced due to increased cell concentrations.

Adult↗
PubMed1987

[Changes in the leukocyte phagocytic activity of donor blood after its UV irradiation. I. Its relation to the irradiation dose and initial level of phagocytic activity].

Phagocytic activity of human mono- and granulocytes increased markedly after UV blood irradiation in the apparatus "Izolda" used in hospitals of the USSR for medical treatment. With the rise of irradiation dose the ratio of cells ingesting latex particles increased, although the average number of particles ingested per cell decreased. The integrative phagocytic index poorly depended on the irradiation dose. In patients with a low initial level of phagocytic index, after UV blood irradiation it became more pronounced than in those with the initial elevated level. The enhancement of phagocytic activity is the result of a direct UV-stimulation of cells. This stimulation not mediated by irradiated blood plasma is known to inhibit the phagocytic activity of leucocytes. A possible mechanism of phagocytic activity stimulation is discussed.

Blood Donors↗
PubMed1982

A microtechnique for studying chemiluminescence response of phagocytes using whole blood and its application to the evaluation of phagocytes in pregnancy.

Previous investigators have demonstrated that polymorphonuclear neutrophils exhibit intense chemiluminescence (CL) during phagocytosis and the CL response can be used to study the cellular and humoral aspects of the phagocytic process. A microtechnique that used 10 microliters of whole blood as a source of phagocytes was developed and used to measure the phagocytic CL response during pregnancy. Increased sensitivity was achieved by the use of a high concentration of luminol (0.5 mM), prepared by sonication, as a CL amplifier. The high intensity of CL produced with luminol permitted the use of a scintillation counter in the IN coincidence mode, avoiding the necessity of dark-adapting the counting vials and reagents and working under subdued red light. The CL response was dose dependent on the number of phagocytes and/or particles (polystyrene spherules, opsonized zymosan, and E coli). The CL response was decreased by inhibitors that prevent particle uptake (iodoacetate and fluoride), inhibitors that prevent free-radical production (sodium benzoate and superoxide dismutase), and by inhibitors that inactivate myeloperoxidase (cyanide and azide). Results suggested that the phagocytic CL response in our assay system was dependent on O2 activation followed by the activated O2 species reacting with myeloperoxidase and chloride. The new technique was used to demonstrate a progressive increase with gestation in the phagocytic CL response in pregnancy and a rapid decrease to normal values at 1 week postpartum.

Female↗