Disease relevance of Phagocytes

• In association with these functional changes, we observed an increase in cellular contents of phagocyte cytochrome b (a critical component of the superoxide-producing oxidase) and immunoreactive cytochrome b heavy chain (the product of the gene that is defective in X-linked chronic granulomatous disease) [1].
• HIV-1 tropism for mononuclear phagocytes can be determined by regions of gp120 outside the CD4-binding domain [2].
• A gene of the intracellular pathogen Salmonella typhimurium that is required for virulence and intracellular survival was identified and shown to have a role in resistance to defensins and possibly to other microbicidal mechanisms of the phagocyte [3].
• Previous studies from this laboratory have demonstrated that Mycobacterium leprae, an obligate intracellular bacterial parasite, enters human mononuclear phagocytes via complement receptors on these host cells and bacterium-bound C3 [4].
• During the acute phase, LBP can be expected to bind gram-negative bacteria and bacterial fragments and promote the interaction of coated bacteria with phagocytes [5].

Psychiatry related information on Phagocytes

• Growing evidence indicates that amyloid (A beta) deposition and phagocyte activation participate in inflammatory reactions in the brain during the course of Alzheimer's disease [6].
• Therefore, dietary beta-carotene can elevate peripartum concentrations of blood beta-carotene, enhance host defense mechanisms by potentiating lymphocyte and phagocyte function, and decrease the incidence of certain reproductive disorders [7].

High impact information on Phagocytes

• PTX3 acts as a functional ancestor of antibodies, recognizing microbes, activating complement, and facilitating pathogen recognition by phagocytes, hence playing a nonredundant role in resistance against selected pathogens [8].
• Heat shock proteins appear to have been involved in innate immune responses since the emergence of phagocytes in early multicellular organisms and to have been commandeered for adaptive immune responses with the advent of specificity [9].
• During the respiratory burst in phagocytes, H(+) current compensates for electron extrusion by NADPH oxidase [10].
• Cell-surface calreticulin initiates clearance of viable or apoptotic cells through trans-activation of LRP on the phagocyte [11].
• Apoptotic cells induce migration of phagocytes via caspase-3-mediated release of a lipid attraction signal [12].

Chemical compound and disease context of Phagocytes

• Thus, chloroquine enhances the activity of mononuclear phagocytes against C. neoformans by iron-independent, pH-dependent mechanisms and is therapeutic in murine models of cryptococcosis [13].
• Technetium 99m phagocyte scanning in inflammatory bowel disease [14].
• Two lipid A analogs, lipid IVA and Rhodobacter sphaeroides lipid A (RSLA), have been described as LPS-receptor antagonists when tested with human phagocytes [15].
• To combat bacterial infection, phagocytes generate superoxide (O2-) and other microbicidal oxygen radicals [16].
• These data show that the HIV-1 envelope glycoprotein alone can stimulate neurotoxin release by binding to CD4 receptors of mononuclear phagocytes [17].

Biological context of Phagocytes

• Apoptosis disables CD31-mediated cell detachment from phagocytes promoting binding and engulfment [18].
• SM-FeSV does not induce haematopoietic malignancies in spite of the fact that its viral oncogene, v-fms, codes for a glycoprotein related to the receptor for the mononuclear phagocyte colony stimulating factor, CSF-1 [19].
• It has been suggested that the macrophage Fc receptor (FcR) provides an efficient route of entry of virus through the attachment of non-neutralized virus-antibody complexes and that for those viruses that escape destruction by the phagocyte, antibody results in a paradoxical increase in virus replication [20].
• Mannose binding protein (MBP) enhances mononuclear phagocyte function via a receptor that contains the 126,000 M(r) component of the C1q receptor [21].
• As increases in cytosolic Ca(2+) concentration (¿Ca(2+)(c)) promote phagocyte antimicrobial responses, we hypothesized that CR phagocytosis of M. tuberculosis is accompanied by altered Ca(2+) signaling [22].

Anatomical context of Phagocytes

• These results indicate that MFG-E8 secreted from activated macrophages binds to apoptotic cells, and brings them to phagocytes for engulfment [23].
• Professional phagocytes, such as neutrophils and monocytes, have an NADPH oxidase that generates superoxide and other reduced oxygen species important in killing microorganisms [24].
• Recent progress in our understanding of the regulation of the phagocyte NADPH oxidase by the Rac GTP-binding protein(s) has provided the first detailed glimpse into the mechanisms of leukocyte regulation by a small GTP-binding protein [25].
• These findings thus indicate that the blood monocyte and tissue macrophage represent an important source of prostaglandin E, a function shared by both normal and neoplastic mononuclear phagocytes [26].
• Mechanisms of phosphatidylserine exposure, a phagocyte recognition signal, on apoptotic T lymphocytes [27].

Associations of Phagocytes with chemical compounds

• Although expression of the c-fms product (CSF-1 receptor) is normally restricted to cells of the mononuclear phagocyte series, the v-fms-coded glycoprotein can contribute to proliferative abnormalities of multiple hematopoietic lineages [28].
• The enzyme NADPH oxidase in phagocytes is important in the body's defence against microbes: it produces superoxide anions (O2-, precursors to bactericidal reactive oxygen species) [29].
• CO drove ischemic protection by activating soluble guanylate cyclase and thereby suppressed hypoxic induction of the gene encoding plasminogen activator inhibitor-1 (PAI-1) in mononuclear phagocytes, which reduced accrual of microvascular fibrin [30].
• Rap1A was found to form stoichiometric complexes with the cytochrome b558 component of the phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system [31].
• Phagocyte impotence caused by an invasive bacterial adenylate cyclase [32].

Gene context of Phagocytes

• Septin: a factor in plasma that opsonizes lipopolysaccharide-bearing particles for recognition by CD14 on phagocytes [33].
• Our results suggest that FPRL1 mediates phagocyte migration in response to SAA [34].
• The chemokine beta family is comprised of at least six distinct cytokines that regulate trafficking of phagocytes and lymphocytes in mammalian species; at least one of these, macrophage inflammatory protein 1 alpha (MIP-1 alpha), also regulates the growth of hematopoietic stem cells [35].
• Involvement of p40phox in activation of phagocyte NADPH oxidase through association of its carboxyl-terminal, but not its amino-terminal, with p67phox [36].
• We found that the chemotactic bacterial peptide, N-formyl- methionyl-leucyl-phenylalanine (fMLP), was able to specifically attenuate Ca2+ mobilization in human phagocytes induced by SAA, but only at very high concentrations, suggesting that SAA uses a low affinity fMLP receptor [34].

Analytical, diagnostic and therapeutic context of Phagocytes

• Cytosolic components of the phagocyte reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase were detected by immunoblotting and immunocytochemical analyses with antibodies against p47-phox and p67-phox [37].
• Immunohistochemistry localized iNOS in phagocytes within the muscularis [38].
• Ligation of PSR by PS on AC surfaces is considered essential for signaling uptake of ACs that are tethered to phagocytes via other receptors [39].
• Using a combination of immunoprecipitation, pharmacologic inhibition, and genetic deletion, we determined that CD44-mediated phagocytosis involves Syk, Rac1, and phosphatidylinositol 3-kinase and induced activation of the phagocyte oxidase [40].
• Targeted inhibition of this oxidase, which is distinct from the phagocyte NADPH oxidase, should provide a new avenue for in vivo therapy aimed at protecting organs at risk from ischemia/reperfusion injury.-Ozaki, M., Deshpande, S [41].

References