No abstract available.
Fetal Blood* ; Humans* ; Oxygen* ; Phagocytes*

The clearance of apoptotic cells is an essential process for tissue homeostasis. To this end, cells undergoing apoptosis must display engulfment signals, such as ‘find-me' and ‘eat-me' signals. Engulfment signals are recognized by multiple types of phagocytic machinery in phagocytes, leading to prompt clearance of apoptotic cells. In addition, apoptotic cells and phagocytes release tolerogenic signals to reduce immune responses against apoptotic cell-derived self-antigens. Here we discuss recent advances in our knowledge of engulfment signals, the phagocytic machinery and the signal transduction pathways for apoptotic cell engulfment.
Apoptosis ; Autoantigens ; Homeostasis ; Phagocytes ; Signal Transduction

Fever has been recognized as a cardinal feature of disease since antiquity, but only recently has the pathophysiology of fever come to be understood. It became clear that the ultimate cause of fever is not a bacterial product (a so-called exogenous pyrogen) but a product of host inflammatory cells (i.e., an endogenous pyrogen). Many studies have demonstrated that mononuclear phagocytes are the principal source of endogenous pyrogen and that a variety of mononuclear cell products can mediate the febrile response. Cytokines are also important as mediators of the acute-phase response to infection and inflammation.
Acute-Phase Reaction ; Cytokines ; Fever* ; Inflammation ; Phagocytes

Neutrophils are the most abundant white blood cells in the peripheral blood and have long been recognized as the major phagocytes in acute infection by destroying extracellular pathogens. Although research on neutrophils hampered by intractability in the experiments, the newly discovered effector functions of neutrophils includes granular proteins, and cytokines, extracellular traps. With all effector mechanism neutrophils play a critical role in the pathogenesis of acute and chronic infection, autoimmunity and cancer.
Autoimmunity ; Cytokines ; Inflammation ; Leukocytes ; Neutrophils ; Phagocytes ; Proteins

Extracellular vesicles (EVs) are membrane-derived vesicles that mediate intercellular communications. As professional phagocytes, neutrophils also produce EVs in response to various inflammatory stimuli during inflammatory processes. Neutrophil-derived EVs can be categorized into 2 subtypes according to the mechanism of generation. Neutrophil-derived trails (NDTRs) are generated from migrating neutrophils. The uropods of neutrophils are elongated by adhesion to endothelial cells, and small parts of the uropods are detached, leaving submicrometer-sized NDTRs. Neutrophil-derived microvesicles (NDMVs) are generated from neutrophils which arrived at the inflammatory foci. Membrane blebbing occurs in response to various stimuli at the inflammatory foci, and small parts of the blebs are detached from the neutrophils, leaving NDMVs. These 2 subtypes of neutrophil-derived EVs share common features such as membrane components, receptors, and ligands. However, there are substantial differences between these 2 neutrophil-derived EVs. NDTRs exert pro-inflammatory functions by guiding subsequent immune cells through the inflammatory foci. On the other hand, NDMVs exert anti-inflammatory functions by limiting the excessive immune responses of nearby cells. This review outlines the current understanding of the different subtypes of neutrophil-derived EVs and provides insights into the clinical relevance of neutrophil-derived EVs.
Blister ; Endothelial Cells ; Extracellular Vesicles* ; Hand ; Ligands ; Membranes ; Neutrophils* ; Phagocytes

Autophagy is a highly conserved intracellular degradation and energy-recycling mechanism that contributes to the maintenance of cellular homeostasis. Extensive researches over the past decades have defined the role of autophagy innate immune cells. In this review, we describe the current state of knowledge regarding the role of autophagy in neutrophil biology and a picture of molecular mechanism underlying autophagy in neutrophils. Neutrophils are professional phagocytes that comprise the first line of defense against pathogen. Autophagy machineries are highly conserved in neutrophils. Autophagy is not only involved in generalized function of neutrophils such as differentiation in bone marrow but also plays crucial role effector functions of neutrophils such as granule formation, degranulation, neutrophil extracellular traps release, cytokine production, bactericidal activity and controlling inflammation. This review outlines the current understanding of autophagy in neutrophils and provides insight towards identification of novel therapeutics targeting autophagy in neutrophils.
Autophagy ; Biology ; Bone Marrow ; Extracellular Traps ; Homeostasis ; Inflammation ; Neutrophils ; Phagocytes

Intraocular silicone oil is known to induce irreversible histological changes in retina. We enucleated an eyeball which was filled with silicone oil for 6 years following pars plana vitrectomy for the treatment of proliferative vitreoretinopathy. Purified 1000 cs silicone oil was used. The reattached retina tissue was examined histopathologically and immunohistochemically. Microscopic examination revealed severe retinal degenerations with many vaculoes in inner retina, the proliferation of glial cells, and the presence of phagocytes. The proliferation of the retinal pigment epithelium and the localized calcification of retinal tissues were also observed. Immunohistochemical study showed retinal tissue expressions of vimentin, S-100, and glial fibrillary acidic protein(GFAP). Electron microscopic examination of the retinal tissues demonstrated some phagocytes with large vacules, which probably had been filled with silicone oil. Our study confirmed that intravitreal silicone oil might damage the retinal tissues.
Neuroglia ; Phagocytes ; Retina* ; Retinal Degeneration ; Retinal Pigment Epithelium ; Retinaldehyde ; Silicone Oils* ; Vimentin ; Vitrectomy ; Vitreoretinopathy, Proliferative

Chronic granulomatous disease(CGD) is a rare inherited disorder of phagocytic cells which results in a susceptibility to infections by catalase-positive bacteria and fungi, as well as granuloma formation. And acute poststreptococcal glomerulonephritis(APSGN) is one of the most common glomerular lesions of gross hematuria in children. We experienced a case of APSGN accompanied with CGD presenting with a liver granuloma.
Bacteria ; Child ; Fungi ; Glomerulonephritis* ; Granuloma ; Granulomatous Disease, Chronic* ; Hematuria ; Humans ; Liver ; Phagocytes

Chronic granulomatous disease(CGD) is a rare inherited disorder of phagocytic cells which results in a susceptibility to infections by catalase-positive bacteria and fungi, as well as granuloma formation. And acute poststreptococcal glomerulonephritis(APSGN) is one of the most common glomerular lesions of gross hematuria in children. We experienced a case of APSGN accompanied with CGD presenting with a liver granuloma.
Bacteria ; Child ; Fungi ; Glomerulonephritis* ; Granuloma ; Granulomatous Disease, Chronic* ; Hematuria ; Humans ; Liver ; Phagocytes

OBJECTIVE: We have previously shown that DICAM inhibits LPS-mediated macrophage differentiation. However, less is known about the exact action mechanisms of DICAM on the macrophage function and differentiation. METHODS: To induce differentiation into a resting M0 macrophage, THP-1 cells were cultured with 100 nM PMA for 24 h, and then rested for 3 days. THP-1 cells were infected with 50 moi of control LacZ- or DICAM-containing adenovirus. The RNA expression profile associated with DICAM during THP-1 differentiation was analyzed with a microarray chip and in silico analysis with Ingenuity Pathway Analysis (IPA) program. RESULTS: A disease and function analysis of the microarray data in DICAM-overexpressed THP-1 cells revealed a suppression in the expression of multiple genes involved in the response of myeloid cells and phagocytes, and an increase of genes associated with apoptosis of fibroblast cell-line, and viral infection and replication. The canonical pathway analysis also showed the most prominent changes of signaling pathways that involve inflammation responses. An upstream regulator analysis identifyingmolecules upstream of the genes that potentially explain the observed expression changes revealed that IRF7 and the genes in type 1 interferon system, such as IFNA2 and IFNAR,was significantly attenuated by DICAM. A mechanistic network analysis confirmed a direct causal association between IRF7 and type 1 interferon system. A real-time RT-PCR analysis validating the microarray data verified the significant suppression of IRFs, IFNA2, and IFNB1. CONCLUSION: These results suggest that DICAM can be a critical regulator of type 1 interferon system, which is an essential mediator in the process of intracellular infection and systemic lupus erythematosus.
Adenoviridae ; Apoptosis ; Computer Simulation ; Fibroblasts ; Inflammation ; Interferons* ; Lupus Erythematosus, Systemic ; Macrophages* ; Myeloid Cells ; Phagocytes ; RNA