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At least 109 records · Page 6Linked to original sources
PubMed1998

Quantifying rat pulmonary intravascular mononuclear phagocytes.

Cells of the mononuclear phagocyte system (MPS) protect the host by clearing effete and foreign particulates from the circulation. The current study was designed to identify, quantify, harvest, and provide a partial functional characterization of the systemic host-defense cell located in the pulmonary microvasculature of the rat. Critical colloid doses of test particulates (monastral blue B [MBB] or polystyrene beads) were infused intra-arterially into anesthetized rats so that phagocytically active pulmonary intravascular phagocytes could be identified. Morphologic characterization of in situ phagocytes was performed using electron microscopy. The number of active phagocytes was then determined using tissue samples processed for light microscopy. Finally, sequential perfusion of the pulmonary vasculature with buffer, chelating agent, and collagenase allowed elution and preliminary functional characterization of the pulmonary intravascular mononuclear phagocyte (PIMP). Electron microscopy demonstrated that both mononuclear phagocytes and neutrophils contributed to pulmonary sequestration of circulating particulates. Light microscopy showed that the microvasculature of each alveolus contained 0.50+/-0.19 active mononuclear phagocytes and 0.14+/-0.12 active neutrophils. A chelation/collagenase elution technique was then used to harvest the PIMP. Histologic evaluation of the postperfusion lungs indicated that 80% of the active phagocytes were removed by the technique. In total, the elution fluids contained 2.63+/-1.04 x 10(7) cells, with 1.60+/-0.78 x 10(7), 0.49+/-0.17 x 10(7), and 0.54+/-0.26 x 10(7) of those cells being mononuclear phagocytes, neutrophils, and lymphocytes, respectively. Functionally, the mononuclear phagocyte population exhibited a spectrum of phagocytic activities, with 51.5+/-19.5% of the cells being inactive, 33.9+/-13.4% exhibiting moderate phagocytic activity, and 14.6+/-9.8% demonstrating intensive phagocytic capacity. The current study provides the first quantified demonstration that mononuclear phagocytes are primarily responsible for sequestering blood-borne foreign particulates in the pulmonary circulation of the rat. Approximately 2 x 10(7) PIMP existed in the lungs of 300 gram rats. The functionally heterogeneous mononuclear phagocytes exhibited phagocytic capacities ranging from avidly phagocytic (14.6+/-9.8%) through moderately active (33.9+/-13.4%) to inactive. The lung microvasculature's large pool of inactive mononuclear phagocytes may provide a recruitable mechanism to allow significant increases in clearance of circulating particulates. A resident pool of activatable mononuclear phagocytes might explain previous clinical observations of increased particulate localization in the lung microvasculature of septic patients.

Animals↗
PubMed2003

Study on the effect of polybutyl-2-cyanoacrylate nanoparticles and their metabolites on the phagocytic activity of peritoneal exudate cells of mice.

The phagocytic activity of peritoneal exudate cells (PECs) harvested from peritoneal cavity of mice after a single intraperitoneal (i.p.) treatment with poly(butylcyanoacrylate) nanoparticles (PBCN) and their probable metabolites [poly(cyanoacrylic acid) (PCAA) and n-butanol] was investigated in an in vitro phagocytic assay. Polymer suspension of PBCN was given as a single i.p. injection at doses of 200 and 10 mgkg(-1), 3, 18, 72 and 120 h before the performance of the phagocytic assay. PCAA and n-butanol were given at the same manner at doses of 126.8 and 96.8 mgkg(-1), respectively (equivalent to a dose of 200 mgkg(-1) of intact PBCN after enzyme hydrolysis) 3, 18 and 120 h before the test performance. The phagocytic assay was performed in vitro in tubes with sheep red blood cells (SRBC). Phagocytic index (percentage of PECs ingested more than 3 sheep erythrocytes), phagocytic number, and ingestion capacity (number of erythrocytes ingested per cell) were the parameters used for evaluation of the phagocytic activity. The alterations of phagocytic activity of the PECs observed were strongly time- and dose-dependent. Administration of all tested compounds shortly before the test performance resulted in a considerable decrease in the capability of PECs to ingest SRBC. The alterations of phagocytic activity decreased when the time between the treatment of mice and the phagocytic assay is on the increase. The dose of 200 mgkg(-1) of PBCN administered 120 h before the phagocytic assay led to the significant increase of the phagocytic index of PECs. The phagocytic function of assayed PECs was temporary impeded and 5 days were completely enough for their restoration.

Animals↗
PubMed1981

Phagocytosis requires repeated triggering of macrophage phagocytic receptors during particle ingestion.

The phagocytic functions of polymorphonuclear leukocytes and mononuclear phagocytes are crucial elements in host defence against a variety of invading microorganisms. Phagocytosis is a highly selective process, requiring specific interactions between the surface of the particle to be ingested and the plasma membrane of the phagocytic cell. The phagocyte can therefore discriminate between 'ingestible' and 'non-ingestible' particles even when the different particles are located in close proximity on the plasma membrane of the phagocytic cell. Previous work has demonstrated that these specific interactions between particle and phagocyte are required not only for the initiation of phagocytosis--that is, attachment of the particle to the phagocytic cells and generation of a signal to trigger phagocyte pseudopod extension--but also for the subsequent progression of pseudopods over the entire surface of the particle. We present evidence here that the continued interactions between phagocyte plasma membrane receptors and particle-bound ligands do not function merely to direct otherwise random phagocyte pseudopod movement, but instead are required for the repeated generation of intracellular phagocytic signals during the entire ingestion process.

Animals↗
PubMed2005

Cholesterol-induced apoptotic macrophages elicit an inflammatory response in phagocytes, which is partially attenuated by the Mer receptor.

Macrophage apoptosis and the ability of phagocytes to clear these apoptotic cells are important processes in advanced atherosclerosis. Phagocytic clearance not only disposes of dead cells but usually elicits an anti-inflammatory response. To study this process in a model of advanced lesional macrophage death, macrophages rendered apoptotic by free cholesterol loading (FC-AMs) were incubated briefly with fresh macrophages ("phagocytes"). FC-AMs were promptly ingested by the phagocytes, which was dependent upon actin polymerization and the phagocyte Mer receptor. Surprisingly, this brief exposure to FC-AMs triggered a modest proinflammatory response in the phagocytes: tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1beta were induced, whereas the levels of transforming growth factor-beta and IL-10 were not increased. This response required cell contact between the FC-AMs and phagocytes but not FC-AM ingestion. TNF-alpha and IL-1beta induction required one or more proteins on the FC-AM surface and was dependent on signaling through extracellular signal-regulated kinase-1/2 mitogen-activated protein kinase and nuclear factor-kappaB in the phagocytes. TNF-alpha production was markedly greater when Mer-defective phagocytes were used, indicating that Mer attenuated the inflammatory response. Interestingly, a more typical anti-inflammatory response was elicited when phagocytes were exposed to macrophages rendered apoptotic by oxidized low density lipoprotein or UV radiation. Thus, the proinflammatory milieu of advanced atherosclerotic lesions may be promoted, or at least not dampened, by contact between FC-induced apoptotic macrophages and neighboring phagocytes prior to apoptotic cell ingestion.

Adaptor Proteins, Signal Transducing↗
PubMed2003

[Phagocytic activity of peripheral blood leukocytes during acute myocardial infarction].

INTRODUCTION: Coronary occlusion may cause acute myocardial infarction associated with many cellular and humoral disturbances of the immune system. The aim of this investigation was to examine phagocytic activity of peripherial blood monocytes and neutrophils as potential cellular markers of systemic immunological events in acute myocardial infarction. MATERIAL AND METHODS: This study included thirty patients following first acute myocardial infarction and thirty healthy volunteers. Immunological analyses were performed on admission and repeated on the second and seventh days after the acute event. Monocytes and neutrophils were obtained from heparinized whole blood after centrifugation and separation on density gradient and incubated with fixed number of heat inactivated and painted particles of yeast. We investigated the following parameters of phagocytic activity: percentage of phagocytosis, phagocytic index, absolute phagocytic index, phagocyte count in a fixed volume of peripherial blood and phagocytic capacity. RESULTS: Except phagocytic index, all phagocytic parameters of monocytes and neutrophils were increased in acute myocardial infarction patients on admission and on the second day of hospitalization. On the seventh day after acute event only the mononuclear phagocyte count in fixed volume of peripheral blood showed significant increase in acute myocardial infarction patients, while percentage of phagocytosis, phagocyte count in fixed volume of peripheral blood and phagocyte capacity of neutrophils were increased during the whole investigated period. CONCLUSION: These data suggest that acute myocardial infarction was followed with strong systemic inflammatory response to myocardial damage. Furthermore, activated monocytes and neutrophils could be a significant source of free radicals, which might be involved in lipid peroxidation and cause tissue damage in early postinfarction period.

Adult↗
PubMed2005

Tramadol does not impair the phagocytic capacity of human peripheral blood cells.

PURPOSE: The inhibitory effect of opioids on phagocytic cell capacity is well established. However, the effect of synthetic analgesics on this aspect of cell function is controversial. It was the aim of the study to compare the in vitro effect of tramadol with that of morphine on the engulfing ability of peripheral blood phagocytic cells from healthy volunteers. METHODS: Peripheral blood polymorphonuclear cells and monocytes from healthy volunteers were incubated with 5, 10 and 20 microg.mL(-1) tramadol, or with 20, 40 and 80 etag.mL(-1) morphine. To each tube, 0.05 mL of 5% suspension of latex beads 0.8 microm in diameter was added. After incubation for 60 min the percentage of cells engulfing latex particles and the phagocytic index (number of particles phagocytized by each individual cell) were detected. RESULTS: Tramadol affected neither the percentage of cells phagocyting latex particles, nor the phagocytic index of both polymorphonuclear cells and monocytes. On the other hand, incubation with 20, 40 and 80 etag.mL(-1) morphine caused 11%, 14% and 24% decrease in phagocytosis (P < 0.01 - P < 0.001). The percentage of monocytes phagocyting latex particles was lower by 16%, 19% and 12% at the three doses tested (P < 0.01 - P < 0.001). The three doses of morphine caused a dose dependent decrease in the monocyte phagocyting index by 20%, 29% and 35.5% respectively (P < 0.05). The polymorphonuclear phagocyting index was not significantly lower following incubation with the drug (P = 0.053). CONCLUSION: The lack of noxious effect of tramadol on the engulfing capacity of phagocytic cells suggests additional benefit to the relatively safe profile of the drug.

Analgesics, Opioid↗
PubMed1990

Phagocyte oxidative metabolism in cyclosporine- or placebo-treated patients with insulin-dependent (type I) diabetes mellitus of recent onset.

Several lines of evidence suggest that phagocyte-mediated oxidative processes are involved in damage to pancreatic islet cells of Type I insulin-dependent diabetes mellitus (IDDM). This hypothesis, however, has not yet been explored at the clinical onset of IDDM. Similarly, the possibility that cyclosporine A (Cy-A) might exert a selective influence on these phagocyte-mediated oxidative reactions has also not yet been investigated as compared to a placebo. The present study tested both hypotheses in 32 patients with recently diagnosed IDDM who were part of the recent French multicenter randomized therapeutic trial of Cy-A. The production of reactive oxygen intermediates (ROI) by circulating polymorphonuclear (PMN) and mononuclear (MN) phagocytes was determined by luminol-dependent chemiluminescence (CL), both directly within microamounts of whole blood and in purified PMN or MN phagocyte suspensions. Lastly, CL production was measured in the absence (resting CL) and the presence of a panel of particular and soluble phagocyte membrane-stimulating agents. We found that on entry into the trial, i.e. within less than 2 months of the clinical onset of IDDM, patients had normal whole blood CL production in the absence of a stimulating agent and upon phagocytic challenge with latex or opsonised zymosan particles. By contrast, whole blood CL responses to soluble stimuli such as phorbol myristate acetate (PMA), concanavalin A (Con-A) and F Met-Leu-Phe (FMLP) were significantly higher than in the control group of 52 normal subjects (P less than 0.01). In purified PMN and MN phagocyte suspensions, both resting and stimulated CL productions were normal, regardless of the type of stimulating agent. After 3 months of treatment, whole blood CL responses to Con-A and FMLP returned to almost normal levels in patients treated with Cy-A (15 cases) but not in those receiving the placebo (17 cases); PMA-induced CL responses were also decreased, but this was found in both groups of patients. In purified phagocyte suspensions we detected no effect of Cy-A on PMN, whereas MN phagocytes from Cy-A-treated patients showed reduced CL responses to FMLP but not to other stimuli. Altogether, these results demonstrate for the first time that the capacity of circulating PMN and MN phagocytes to generate ROI is normal at the clinical onset of IDDM and suggest that circulating substances increase oxidative responses to soluble, but not particulate, stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1998

Impaired phagocyte oxidative capacity in patients with human immunodeficiency virus infection.

Bacterial infections that may be related to impaired phagocyte function often develop in patients infected with human immunodeficiency virus (HIV). We examined the oxidative capacity of circulating phagocytes in 78 HIV+ patients and 31 control subjects by measuring chemiluminescence with a whole blood assay. Phagocytes were stimulated with zymosan opsonized with human complement (hC-OPZ) or immunoglobulin (hI-OPZ) with or without exogenous primers. Patients with CD4+ < 500/microL showed reduced whole blood chemiluminescence at maximal opsonin receptor (MOR) activity after priming in response to hC-OPZ relative to control subjects, and the difference was significant for patients with CD4+ < 100/microL. Patients had lower absolute phagocyte counts; however, the chemiluminescence activity calculated per phagocyte count was significantly depressed in advanced HIV infection, indicating the impairment of phagocytic cell function and a reduction in number. Data were similar when hI-OPZ was used as a stimulus. The chemiluminescence of unprimed phagocytes at circulating opsonin receptor (COR) activity relative to maximally primed phagocytes (COR/MOR ratio) was significantly higher for HIV+ patients as compared with control subjects and indicates a defect in phagocyte priming. Alternatively, the phagocytes do not increase chemiluminescence with priming because they have already been primed or activated in vivo. In late-stage disease, decreased opsonin receptor-dependent respiratory burst activity contributes to the risk of secondary bacterial infections.

Adult↗
PubMed1998

Compensation of preliminary blood phagocyte immaturity in the newborn calf.

To estimate the functional maturity of the phagocytic defence in neonatal calves, we analyzed the characteristics of blood phagocytes from calves (n = 10) 1 h post partum (p.p.) and 4 h p.p. At 1 h p.p., all calves were colostrum-deprived, while 5 calves had received colostrum before the 4 h p.p. sampling. The results were compared to those obtained from 3-9-week-old calves (n = 10). Phagocytic and oxidative burst activity of polymorphonuclear leukocytes (PMNL) and monocytes were determined in whole blood and separately analyzed by flow cytometry. In neonates prior to colostrum ingestion (1 h p.p.), phagocytic activity of PMNL against non-preopsonized E. coli was lower when compared to PMNL of 3-9-week-old calves. Opsonization of bacteria with pooled plasma from adult animals only partially restituted this lower PMNL phagocytic activity, indicating that humoral as well as cellular aspects of PMNL phagocytosis are altered in neonatal calves. In contrast to PMNL, monocytes of neonates exhibited an enhanced phagocytic activity. The oxidative burst activity of PMNL, as well as of monocytes was higher in newborn calves. During the first 4 h of life, the activities of blood phagocytes changed. Colostrum ingestion was accompanied by an increase in the percentage of phagocytizing PMNL and monocytes. This increase was absent in colostrum-deprived calves. In contrast, the oxidative burst activity of phagocytes decreased with age. In monocytes, the decrease of oxidative burst activity was only observed in colostrum-fed calves. In conclusion, some blood phagocyte functions in calves were found to be immature at birth, but these functions are presumably compensated by high absolute PMNL numbers and by other the more active mechanisms.

Aging↗