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

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

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

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

A micropipette aspiration technique was adopted in this study on the viscoelastic properties of phagocytes of atherosclerotic origin. A standard linear solid model (Kelvin model) was employed to fit the experimental data, and the 3 viscoelastic coefficients of the model were used to compare the mechanical properties of the phagocytes in different phases during atherosclerosis development. The experimental results indicated that prior to the formation of atherosclerosis, the deformability of the macrophages matured from monocytes decreased, and their rigidity increased. At the initial stage of atherosclerosis formation, the deformability of the foam-cells decreased further. We believe that the deterioration in the deformability of the cells might reduce their mobility within the arterial wall, thus leading to the genesis of atherosclerosis caused by the stagnation and accumulation of the cells laden with atherogenic lipids within the arterial wall. This finding may have important implication in the researches on arteriosclerosis.
Animals ; Atherosclerosis ; pathology ; Elasticity ; Linear Models ; Male ; Monocytes ; pathology ; Phagocytes ; pathology ; Rabbits ; Random Allocation ; Viscosity

Neutrophils are professional phagocytes that conduct effectors functions in the innate immune systems. They are differentiated in the bone marrow (BM) and terminally differentiated neutrophils are then released into systemic circulation. Neutrophils migrate into inflammatory foci through extravasation, reverse transmigration, and chemotaxis. As neutrophils arrive at a target site, they actively participate in eliminating pathogens. They phagocytose bacteria, and eliminate them through the generation of reactive oxygen species (ROS), release of protease-enriched granules, and formation of neutrophil extracellular traps (NETs). Since neutrophils are equipped with toxic arsenals, the activation of neutrophils is tightly controlled. Priming is the process of unlocking safety mechanisms before complete activation of neutrophils. Since the first discovery of neutrophils, they were considered as a homogeneous population with an inflammatory phenotype. However, heterogenous populations of neutrophils were discovered under physiological and pathological conditions. This review outlines the normal differentiation of neutrophils in the BM, and discusses the current understandings of neutrophil heterogeneity.
Bacteria ; Bone Marrow ; Chemotaxis ; Extracellular Traps ; Immune System ; Neutrophils* ; Phagocytes ; Phenotype ; Population Characteristics* ; Reactive Oxygen Species

We present a case of perforating granuloma annulare which appeared as multiple small papular lesions with central umbilication on the dorsum of both foot and sides of foot, The patient was a 12 year-old female child who had slightly tender lesions of one month's duration. Histologic study showed perforation of the epiderrnis and release of the abnormal necrobiotic material transepiderrnally. The epidermal perforation communicated with area of granuloma annulare in the dermis that consist of necrobiotic collagen surrounded by palisading mononucler phagocytes in the dermis. All the lesions resolved spontaneously with a slight hyperpigmentation in 4 months. She also had erythematous tender nodules, which diagnosed as erythema nodosum, on both shins. The lesions responded to potassium iodide 1.0g for 2 weeks.
Child ; Collagen ; Dermis ; Erythema Nodosum ; Female ; Foot ; Granuloma Annulare* ; Granuloma* ; Humans ; Hyperpigmentation ; Phagocytes ; Potassium Iodide

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