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International Journal of Clinical &... 1996Intact phagocyte function is a pre-requisite for successful defence against infection, but paradoxically, these cells may also play a major role in the pathogenesis of...
Intact phagocyte function is a pre-requisite for successful defence against infection, but paradoxically, these cells may also play a major role in the pathogenesis of the infant respiratory distress syndrome. Phagocyte function is known to be deficient in pre-term infants, who are at risk of infection as a result, but these infants are also at risk of respiratory distress syndrome as a result of surfactant deficiency. Despite this, few longitudinal studies of phagocyte function have been performed in pre-term infants. We have used lucigenin-enhanced chemiluminescence to examine the respiratory burst of mixed samples containing polymorphonuclear leucocytes and monocytes of 100 pre-term infants at 48- to 72-h intervals during their admission to a neonatal care unit. Increased polymorphonuclear leucocyte chemiluminescence was associated with respiratory distress syndrome and the use of intermittent positive pressure ventilation. Multiple linear regression analysis revealed a slight, but significant depression of chemiluminescence in association with the use of gentamicin and penicillin when stronger influencing factors such as the presence of respiratory distress syndrome were taken into consideration. Measurement of phagocyte function by sensitive luminescence assays requires very little blood and may be useful in pre-term infants to follow the severity of respiratory distress syndrome. However, it is probable that other factors such as antioxidant capacity also have an important influence on the degree of tissue damage.
Topics: Anti-Bacterial Agents; Bacterial Infections; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Luminescent Measurements; Phagocytes; Respiratory Distress Syndrome, Newborn
PubMed: 8856364
DOI: 10.1007/BF02592353 -
Journal of Leukocyte Biology Jan 2019Phagocytes are cells of the immune system that play important roles in phagocytosis, respiratory burst and degranulation-key components of innate immunity and response... (Review)
Review
Phagocytes are cells of the immune system that play important roles in phagocytosis, respiratory burst and degranulation-key components of innate immunity and response to infection. This diverse group of cells includes monocytes, macrophages, dendritic cells, neutrophils, eosinophils, and basophils-heterogeneous cell populations possessing cell and tissue-specific functions of which cellular metabolism comprises a critical underpinning. Core functions of phagocytic cells are diverse and sensitive to alterations in environmental- and tissue-specific nutrients and growth factors. As phagocytic cells adapt to these extracellular cues, cellular processes are altered and may contribute to pathogenesis. The considerable degree of functional heterogeneity among monocyte, neutrophil, and other phagocytic cell populations necessitates diverse metabolism. As we review our current understanding of metabolism in phagocytic cells, gaps are focused on to highlight the need for additional studies that hopefully enable improved cell-based strategies for counteracting cancer and other diseases.
Topics: Adaptation, Physiological; Animals; Humans; Macrophages; Metabolic Networks and Pathways; Neoplasms; Neutrophils; Phagocytes
PubMed: 30247792
DOI: 10.1002/JLB.4RI0518-195R -
Advances in Experimental Medicine and... 2020Dictyostelium cells are professional phagocytes that are capable of handling particles of variable shapes and sizes. Here we offer long bacteria that challenge the...
Dictyostelium cells are professional phagocytes that are capable of handling particles of variable shapes and sizes. Here we offer long bacteria that challenge the uptake mechanism to its limits and report on the responses of the phagocytes if they are unable to engulf the particle by closing the phagocytic cup. Reasons for failure may be a length of the particle much larger than the phagocyte's diameter, or competition with another phagocyte. A cell may simultaneously release a particle and engulf another one. The final phase of release can be fast, causing the phagosome membrane to turn inside-out and to form a bleb. Myosin-II may be involved in the release by generating tension at the plasma membrane, it does however not accumulate on the phagosome to act there directly in expelling the particle. Labeling with GFP-2FYVE indicates that processing of the phagosome with phosphatidylinositol 3-phosphate begins at the base of a long phagosome already before closure of the cup. The decision of releasing the particle can be made even at the stage of the processed phagosome.
Topics: Bacteria; Dictyostelium; Phagocytes; Phagocytosis; Phagosomes
PubMed: 32399826
DOI: 10.1007/978-3-030-40406-2_5 -
Indian Journal of Pediatrics 1990
Review
Topics: Cell Adhesion; Chemotaxis, Leukocyte; Humans; Infant, Newborn; Macrophages; Neutrophils; Nutrition Disorders; Phagocytes
PubMed: 2246010
DOI: 10.1007/BF02722075 -
Archives of Biochemistry and Biophysics Dec 1994Injury after exposure to mineral oxide dusts is considered to be mediated by free radical generation. In vitro production of hydroxyl radical by a fibrous silicate...
Injury after exposure to mineral oxide dusts is considered to be mediated by free radical generation. In vitro production of hydroxyl radical by a fibrous silicate increases with the [Fe3+] complexed to the dust surface. The study hypothesis tested was that extracellular fluids and phagocytic cells can decrease concentrations of iron complexed to the surface of a fibrous silicate by employing host chelators and reductants. Such a depletion of surface [Fe3+] would predict decrements in both oxidant generation and the resultant injury after inhalation and instillation of these mineral oxides. Crocidolite (2.0 mg) which was exposed to either 5.0 ml rat plasma or 10.0 ml rat lavage fluid for 1 h had diminished surface [Fe3+]. Similarly, incubations of crocidolite (2.0 mg) with either 10.0 ml rat alveolar macrophages (1.0 x 10(6) cells/ml) or 10.0 ml rat neutrophils (1.0 x 10(7) cells/ml) decreased concentrations of surface iron. In vivo exposures of asbestos contained in chambers allowing or precluding inflammatory cell entry revealed that the influx of phagocytes was associated with greater decreases in surface [Fe3+]. The body chelators transferrin and lactoferrin were unable to extract the metal from fiber surface in vitro. However, superoxide generated by phagocytes did displace the iron from the crocidolite surface. We conclude that extracellular fluids and phagocytic cells have a capacity to diminish [Fe3+] complexed to the surface of asbestos and therefore decrease the potential for oxidative stress and injury to a living system after exposure to these dusts.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Animals; Asbestos; Asbestos, Crocidolite; Calcium; Chelating Agents; Epithelium; Ferric Compounds; Macrophages, Alveolar; Magnesium; Male; Neutrophils; Oxidative Stress; Phagocytes; Rats; Rats, Sprague-Dawley; Respiratory Burst; Superoxide Dismutase
PubMed: 7986061
DOI: 10.1006/abbi.1994.1493 -
Annals of the New York Academy of... Dec 2015The relationship between malignant B cells and macrophages has long been established. Furthermore, evolutionary studies have demonstrated that B cells from early... (Review)
Review
The relationship between malignant B cells and macrophages has long been established. Furthermore, evolutionary studies have demonstrated that B cells from early vertebrates have both phagocytic and antibody production capabilities. In addition to their lymphoid nature, B-1 cells retain several myeloid characteristics. Various reports have demonstrated that B-1 cells can differentiate into phagocytes. However, descriptions of B-1 cells as a novel phagocyte cell member are rarely found in the literature. This review aims to present the available data regarding B-1 cell-derived phagocytes and also discusses how their existence might be relevant to hematopoiesis and immune responses.
Topics: Animals; B-Lymphocyte Subsets; Cell Differentiation; Hematopoiesis; Humans; Phagocytes; Phagocytosis
PubMed: 26149496
DOI: 10.1111/nyas.12814 -
Der Pathologe Sep 2015The macrophage cell system was identified by Metchnikoff on the basis of its phagocytic ability. Later on, the reticulohistiocytic system was defined as being composed... (Review)
Review
The macrophage cell system was identified by Metchnikoff on the basis of its phagocytic ability. Later on, the reticulohistiocytic system was defined as being composed of antigen-presenting reticulum cells and macrophages. Van Furth proposed that the mononuclear phagocyte system includes all tissue macrophages as well as antigen-presenting cells and blood monocytes as their precursors. Recent findings have shown that blood monocytes are not just transient forms involved in the recruitment of macrophages but that different dendritic and monocytic subpopulations can be observed in blood. In tissue, self-renewing macrophages derived from the yolk sac as well as monocyte-derived dendritic cells and monocyte-derived macrophages can be distinguished. Due to their plasticity and polarization, under inflammatory conditions monocyte-derived macrophages may be beneficial for the reestablishment of homeostasis or may contribute to mostly chronic diseases. Because of their ubiquitous distribution, monocytes and macrophages are increasingly considered to be possible therapeutic targets.
Topics: Antigen-Presenting Cells; Cell Differentiation; Cell Transformation, Neoplastic; Dendritic Cells; Humans; Macrophages; Monocytes; Phagocytes; Phagocytosis
PubMed: 26310365
DOI: 10.1007/s00292-015-0050-y -
Journal of Autoimmunity Apr 1990Several lines of evidence suggest that phagocyte-mediated oxidative processes are involved in damage to pancreatic islet cells of Type I insulin-dependent diabetes... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
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)
Topics: Adolescent; Adult; Cyclosporins; Diabetes Mellitus, Type 1; Double-Blind Method; Female; Humans; Luminescent Measurements; Luminol; Male; Multicenter Studies as Topic; Neutrophils; Oxygen; Phagocytes; Randomized Controlled Trials as Topic
PubMed: 2187453
DOI: 10.1016/0896-8411(90)90141-e -
Annual Review of Microbiology 1995Nonopsonic phagocytosis mediated by phagocyte receptors that recognize corresponding adhesins on microbial surfaces has attracted increasing interest as a potential host... (Review)
Review
Nonopsonic phagocytosis mediated by phagocyte receptors that recognize corresponding adhesins on microbial surfaces has attracted increasing interest as a potential host defense mechanism against extracellular pathogens and as a means of survival in the host for intracellular pathogens. Three types of nonopsonic phagocytosis involving carbohydrate-protein interactions (also termed lectinophagocytosis), protein-protein interactions, and hydrophobic interactions are discussed. A prominent receptor on phagocytic cells involved in recognizing pathogens belongs to the CD11/CD18 integrins. It mediates both opsonophagocytosis and nonopsonic phagocytosis and exhibits multiple specificity for different microbial adhesins. In other cases, similar specificity toward a microbial ligand (e.g. the Klebsiella pneumoniae capsule) is shared by dual molecules, one of which (e.g. the mannose-binding protein in serum) mediates opsonophagocytosis and the other (e.g. the macrophage mannose receptor) mediates nonopsonic phagocytosis of the microorganisms. In addition, we discuss how nonopsonic phagocytosis can trigger the phagocytes to release inflammatory agents and cause tissue injury. Further studies of the molecular mechanisms of nonopsonic phagocytosis, in particular those underlying the up-regulation of the phagocytic receptors by various agents, should lead to the development of new approaches for the prevention of infectious diseases.
Topics: Amino Acid Sequence; Animals; Bacteria; Carbohydrate Sequence; Eukaryota; Humans; Molecular Sequence Data; Phagocytes; Phagocytosis
PubMed: 8561460
DOI: 10.1146/annurev.mi.49.100195.001323 -
Immunological Reviews Nov 2014Phagocytosis is a remarkably complex and versatile process: it contributes to innate immunity through the ingestion and elimination of pathogens, while also being... (Review)
Review
Phagocytosis is a remarkably complex and versatile process: it contributes to innate immunity through the ingestion and elimination of pathogens, while also being central to tissue homeostasis and remodeling by clearing effete cells. The ability of phagocytes to perform such diverse functions rests, in large part, on their vast repertoire of receptors. In this review, we address the various receptor types, their mobility in the plane of the membrane, and two modes of receptor crosstalk: priming and synergy. A major section is devoted to the actin cytoskeleton, which not only governs receptor mobility and clustering but also is instrumental in particle engulfment. Four stages of the actin remodeling process are identified and discussed: (i) the 'resting' stage that precedes receptor engagement, (ii) the disruption of the cortical actin prior to formation of the phagocytic cup, (iii) the actin polymerization that propels pseudopod extension, and (iv) the termination of polymerization and removal of preassembled actin that are required for focal delivery of endomembranes and phagosomal sealing. These topics are viewed in the larger context of the differentiation and polarization of the phagocytic cells.
Topics: Actin Cytoskeleton; Animals; Cytoskeleton; Humans; Immunological Synapses; Phagocytes; Phagocytosis; Phenotype; Protein Binding; Protein Transport; Receptors, Immunologic; Signal Transduction
PubMed: 25319336
DOI: 10.1111/imr.12212