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At least 19 recordsLinked to original sources
PubMed1994

Physiology and biochemistry: influence of exercise on phagocytosis.

Phagocytic cells constitute the organism's first line of defence against external aggression. These cells carry out their non-specific defence function through what is known as the phagocytic process. This can be split up into several stages: adherence, chemotaxis, attachment, ingestion and killing of the foreign agent. The influence of exercise on the phagocytic process is dependent on the step considered, but in general, different responses have been observed in the adherence and chemotaxis capacities depending both on the intensity of exercise and on the phagocyte (neutrophil or monocyte-macrophage) studied. However, with respect to the attachment and ingestion of antigen, exercise generally induces an increase in every "situation", independent of the intensity of physical activity and the involvement of neutrophils or macrophages. The results with regard to the microbicide capacity that have been obtained up to the present time are very contradictory, showing perhaps a greater dependence on the phagocyte studied and on the intensity of exercise. This fact may be due to different methods used in the studies. One could conclude that exercise stimulates certain stages of the phagocytic process. This stimulation could counterbalance the decreased lymphoid activity after certain types of exercise that some authors have reported.

Biochemical Phenomena↗
PubMed1976

[Effects of histones on phagocytosis and phagocytic metabolism].

Enhanced phagocytosis and no intracellular glycogen breakdown was found in guinea-pig peritoneal polymorphonuclear leukocytes (PMN) incubated together with heat-killed staphylococci (Twort) treated with a calf thymus histone fraction (P II), for 1 hr at 37 degrees C. Glcose consumption and lactate production of these PMN's were as high as in phagocytosis of the same germ untreated with P II, and their oxygen consumption was depressed significantly.

Animals↗
PubMed1996

Effect of phagocytosis of pHEMA particles and of heat-killed Candida albicans on expression of carbohydrate-binding sites such as endogenous lectins in phagocytes.

Phagocytosis of particles is an integral part of the defence system. Besides clearing the environment of foreign material this mechanism may affect the expression of physiologically relevant epitopes such as carbohydrate-binding sites, e.g. lectins. To determine the effect of particle design on the expression of such determinants in human monocytes and peritoneal macrophages either in suspension or after adherence, the binding of labelled (neo)glycoproteins was comparatively studied after exposure to poly (2-hydroxyethyl methacrylate) particles and heat-inactivated Candida albicans cells. A stimulatory effect of phagocytosis on extent of expression of binding sites for (neo)glycoproteins in phagocytic cells was observed. The levels of responsiveness varied according to the type of particle, adherence of the cell adding a further regulatory parameter. These results support the notion of a potential influence of the chemical structure and/or the form of an engulfed particle on phagocyte differentiation.

Binding Sites↗
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↗
PubMed1989

Bacterial adaptation to oxidative stress: implications for pathogenesis and interaction with phagocytic cells.

During phagocytosis, phagocytic cells generate superoxide and other reactive oxygen species, which are involved in antibacterial activity. However, many bacteria possess antioxidant defenses that may explain their survival in inflammatory foci. These defenses include antioxidant enzymes such as superoxide dismutase and catalase, DNA repair systems, scavenging substrates, and competition with phagocytes for molecular oxygen. These defenses are probably coordinated, and different responses occur with different reactive oxygen species. Escherichia coli and Salmonella typhimurium mutants have allowed the demonstration of a variety of critical genes for enzymatic defense and DNA repair, as well as an oxyR regulon system. In more complex systems, the conditions found in inflammatory foci, such as decreasing glucose and the production of lactate, enhance bacterial catalase production and resistance to hydrogen peroxide. Resistance and adaptation to phagocyte-derived oxidant stress are critical aspects of bacterial pathogenesis.

Bacteria↗
PubMed2001

Multiple receptors mediate apoJ-dependent clearance of cellular debris into nonprofessional phagocytes.

Phagocytosis of apoptotic, senescent, and dying cells by macrophages is a well characterized process. More recently it has been shown that in addition to macrophages vital neighboring cells in the affected tissue participate in the cellular clearance. While scavenger receptors have been shown to mediate uptake into macrophages, it is poorly understood how cellular debris is internalized by nonprofessional phagocytes. We here analyze the endocytic activity of vital fibroblasts and epithelial cells exposed to cellular debris and membrane remnants. We show a mutual stimulation in the endocytosis of debris and apolipoproteinJ (clusterin) in these cells. Experiments using RAP (receptor-associated protein) to block ligand binding to LRP and megalin as well as studies in LRP- and megalin-deficient cells suggest that the uptake of apoJ and cellular debris is mediated by megalin, LRP, and yet unidentified internalization mechanisms.

Animals↗
PubMed1984

In vitro evidence for the requirement of filopodial elongation for the progress of phagocytosis by phagocytic granular cells of the silkworm, Bombyx mori.

The significance of filopodial elongation of phagocytic granular cells of Bombyx mori in the progress of phagocytosis was investigated by regulating the degree of filopodial elongation with low temperature and cytochalasin B (CB). Elongation-inhibited cells were unable to ingest foreign cells such as sheep erythrocytes (SRBC), while cells having more or less the ability to elongate their filopodia against SRBC could phagocytose them. The results showed that filopodial elongation was an essential element in the progress of a series of phagocytic processes following attachment, and also suggested that certain level of intracellular phagocytic signals obtained during elongation is required for the completion of phagocytosis.

Animals↗
PubMed2004

Effects of caspofungin (MK-0991) and anidulafungin (LY303366) on phagocytosis, oxidative burst and killing of Candida albicans by human phagocytes.

The objective of the present study was to investigate the influence of the new echinocandins caspofungin (MK-0991) and anidulafungin (LY303366) on human phagocytes. Phagocytosis, oxidative burst and intracellular killing of Candida albicans were analyzed by flow cytometry. Neither caspofungin nor anidulafungin significantly influenced phagocytosis. Only caspofungin significantly influenced oxidative burst after 15 min of incubation ( P<0.05). Both caspofungin and anidulafungin improved intracellular killing rates of C. albicans after 2 h of incubation (42.4% and 43.2%, respectively, compared to 37.9% in controls; P<0.05). In conclusion, caspofungin significantly improves oxidative burst and intracellular killing, which may be advantageous for clinical therapy.

Anidulafungin↗
PubMedDate not supplied

[Phagocytic activity of polymorphonuclear leukocytes of pregnant women].

Cellular and humoral immunity are depressed during pregnancy, for this reason the non-specific immunity mediated by polymorphonuclear leukocytes plays an important role in the defense against bacterial infections. The objective of this study was evaluate the phagocytosis, phagocytic index (particles ingested average by cell) and nitroblue tetrazolium reduction (NBTr) in three trimesters of pregnancy. The phagocytosis and rNBT assays were carried out by means of adherence on surface of the glass. The resulted showed that phagocytosis, phagocytic index and NBTr were normal in two first trimesters of pregnancy compared with nonpregnant women group. However, phagocytosis and phagocytic index were significantly decrease (p < 0.05) in the third trimester pregnancy. This phagocytosis deficiency possibly explains the increase of respiratory infections, diarrhea disease and bacteriuria. Several factors could be responsible of this non-specific immunity depressed during pregnancy. Further studies are necessary to define the biological significance of this immunosuppression.

Adult↗
PubMed2000

Helicobacter pylori inhibits phagocytosis by professional phagocytes involving type IV secretion components.

Gastric infections by Helicobacter pylori are characteristically associated with an intense inflammation and infiltration of mainly polymorphonuclear lymphocytes (PMNs) and monocytes. The inflammatory response by infiltrated immune cells appears to be a primary cause of the damage to surface epithelial layers and may eventually result in gastritis, peptic ulcer, gastric cancer and/or MALT-associated gastric lymphoma. Our analysis of the interaction between H. pylori and PMNs and monocytes revealed that H. pylori inhibits its own uptake by these professional phagocytes. To some degree, this effect resembles antiphagocytosis by Yersinia enterocolitica. Increasing numbers of bacteria associated per cell are more efficient at blocking their own engulfment. In H. pylori, bacterial protein synthesis is necessary to block phagocytic uptake, as shown by the time and concentration dependence of the bacteriostatic protein synthesis inhibitor chloramphenicol. Furthermore, H. pylori appears broadly to inhibit the phagocytic function of monocytes and PMNs, as infection with H. pylori abrogates the phagocytes' ability to engulf latex beads or adherent Neisseria gonorrhoeae cells. This antiphagocytic phenotype depends on distinct virulence (vir) genes, such as virB7 and virB11, encoding core components of a putative type IV secretion apparatus. Our data indicate that H. pylori exhibits an antiphagocytic activity that may play an essential role in the immune escape of this persistent pathogen.

Bacterial Adhesion↗
PubMed1988

Cellular defense of the avian respiratory system: influx and nonopsonic phagocytosis by respiratory phagocytes activated by Pasteurella multocida.

Poultry have a very limited number of resident macrophages in the normal steady-state respiratory tract. Thus, poultry must rely heavily on active migration of phagocytic cells to the lungs and air sacs in defending against respiratory pathogens. Intratracheal administration of a live, apathogenic Pasteurella multocida vaccine (Choloral; Clemson University strain) increased the number of avian respiratory phagocytes (ARP; obtained by lavage of lungs and air sacs) within 24 h by 3 orders of magnitude compared with the number of ARP obtained from mock-inoculated controls and from nonreacting chickens. Chickens yielding a high number of ARP did not show any sign of respiratory disease. Flow cytometric analysis of ARP that were exposed to 20 nonopsonized fluorescent microspheres per ARP for 30 min at 37 degrees C demonstrated a fivefold increase in the percentage of actively phagocytic cells in the ARP populations of stimulated chickens compared with the percentage of phagocytic ARP for mock-inoculated control birds. The phagocytic capacity (relative number of engulfed microspheres) of ARP from stimulated birds doubled during the same time. The flow cytometric observations were confirmed by fluorescence microscopy. These results indicate that activation by avirulent replicating agents of phagocytic cells of chicken to migrate to the respiratory tract may be a means of defending poultry against air sacculitis and pneumonia.

Animals↗
PubMed1996

Role of reactive oxygen metabolites in murine peritoneal macrophage phagocytosis and phagocytic killing.

This study was designed to quantify the role of reactive oxygen metabolites (ROMs) in two distinct components of murine peritoneal macrophage activity, phagocytosis and killing, and to discriminate quantitatively the degree to which each component is dependent on NADPH oxidase and/or xanthine oxidase. A fluorochromatic vital staining technique was modified to simultaneously quantify phagocytosis and microbicidal activity of macrophages incubated with Candida parapsilosis targets. To determine the role of ROMs, macrophages were preincubated with free radical scavengers [superoxide dismutase (SOD) and/or catalase] or with selective inhibitors of xanthine oxidase (XO, e.g., allopurinol) or NADPH oxidase [diphenyleneiodonium (DPI)]. Phagocytosis was not affected by treatment of macrophages with SOD, catalase, allopurinol, or DPI. Candidacidal activity, however, was inhibited by SOD, allopurinol, or DPI. The inhibitory effects of DPI and allopurinol were additive. Histochemical and biochemical assays demonstrated substantial quantities of XO in murine peritoneal macrophages. The findings suggest that the generation of ROMs by XO- and NADPH oxidase-dependent pathways are each important for phagocytic killing by murine peritoneal macrophages.

Allopurinol↗
PubMed1982

[Phagocytes and phagocytosis 100 years after Metchnikoff. A current picture of the neutrophil leukocyte].

The observation of the amoebocytes of primitive organisms led ELIAS METSCHNIKOFF in 1882 to the idea that blood phagocytes--neutrophilic leukocytes in particular--could constitute an anti-microbial defense system. This was the beginning of the phagocyte theory which METSCHNIKOFF developed over many years and which in essence is still valid. The author sets out to provide an updated view of the neutrophil. Circulating neutrophils are end-cells. They develop in the bone marrow by a relatively long maturation process during which the characteristic azurophil and specific granules are formed. The granules are stored organelles. The azurophil granules contain microbicidal enzymes, i.e. myeloperoxidase and lysozyme, together with a large number of acid hydrolases and neutral proteases. The specific granules contain lysozyme, a collagenase, lactoferrin and transcobalamines. By subcellular fractionation a third kind of storage organelle has recently been found which is characterized by its gelatinase content. Circulating neutrophils are activated on microbial invasion--first in the blood, by chemotactic factors formed at the site of infection, and subsequently by the microbes themselves which are phagocytosed by the immigrating neutrophils. Chemotactic factors lead to directed migration and induce the secretion of enzymes which presumably facilitate this process. Phagocytosis results in the mobilization of neutrophil products in large quantities. The contact between the cell and the microorganism activates in the neutrophil membrane an oxidase which produces superoxide, and a phospholipase which releases arachidonic acid. The latter is then oxidized by cyclooxygenase and lipoxygenase. There is also massive liberation of enzymes from all three storage compartments. The production of superoxide is the essential process for the killing of a large variety of microorganisms.

Allergy and Immunology↗
PubMed1998

Endothelial cells potentiate oxidant-mediated Kupffer cell phagocytic killing.

Phagocytosis and killing of circulating organisms by Kupffer cells (KCs) are discrete, important components of host defense. However, the killing mechanism(s) are not fully understood, and the potential role of adjacent nonparenchymal cells such as hepatic endothelial cells has not been defined. Rat KCs -/+ an hepatic endothelial cell enriched cellular fraction (HECEF) were incubated with Candida parapsilosis and assayed for phagocytosis and phagocytic killing by validated fluorochromatic vital staining. The role of reactive oxygen metabolites in KC phagocytic functions was examined by inhibition with superoxide dismutase and/or catalase. Diphenyleneiodonium and allopurinol were used to examine the potential roles of NADPH oxidase and xanthine oxidase, respectively, in generating these toxic oxidants. Coculture with HECEF increased KC phagocytic activity (from 75% to 88%) and candidacidal activity (from 20% to 31%). Superoxide dismutase, catalase, diphenyleneiodonium, or allopurinol caused inhibition of candidacidal activity, but did not affect phagocytosis, and did not block the potentiation of phagocytosis or of killing caused by coculture with HECEF. Reactive oxygen intermediates generated by both NADPH oxidase and xanthine oxidase-dependent pathways are important in KC killing of Candida parapsilosis. In vitro, KC phagocytosis and killing are potentiated (via a non-oxidant-mediated mechanism) by coculture with a preparation of hepatic non-parenchymal cells composed primarily of endothelial cells.

Allopurinol↗