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Pathogenicity and Virulence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
The ingestion of a microorganism by a phagocyte results in the formation of a phagosome, and if the microbe had been appropriately opsonised, as with LgG antibodies, an oxidative burst occurs. If the phagocyte is a macrophage that had been activated by IFN-gamma, the formation of reactive nitrogen intermediates (RNT) is also induced. Under normal conditions the phagosome fuses with lysosomes to form a phagolysosome. The microbicidal systems of the phagocyte are contained within the phagosomes and lysosomes. Any microorganism that has the ability to interfere with these processes therefore enhances its chances of intracellular survival.
Immune Function in Exercise-Induced Injuries
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
Louis C. Almekinders, Sally V. Almekinders
Following the initial generation of vasoactive, pro-inflammatory mediators, cellular elements are recruited to the area of injury. Both neutrophils, monocytes/macrophages, as well as lymphocytes, are recruited to the area. Chemotactic factors, such as complement-derived C5a and leukotriene B4, result in margination of inflammatory cells along vascular walls at the site of injury. After adherence and migration through the vascular wall, the inflammatory cells can be activated to perform their phagocytic function. The activation or stimulus-response coupling within the neutrophil appears to be regulated through changes in intracellular calcium, activation of phospholipase and protein kinase.20,21 After activation, clearance of injured and necrotic tissues can commence. Initial engulfment by the neutrophil cell membrane of the necrotic debris results in the formation of a phagosome. After fusion with lysosomes, the proteolytic enzymes can complete the degradation in the phagolysosome.
The Injured Cell
Published in Jeremy R. Jass, Understanding Pathology, 2020
These membrane bound structures contain hydrolases such as proteases (e.g. cathepsin G), lipases and glucosidases. They are very numerous in phagocytic cells, neutrophils and macrophages. Phagocytosed bacteria are digested when the phagosome fuses with lysosomes to form a phagolysosome.
Melanocortin 5 Receptor Expression and Recovery of Ocular Immune Privilege after Uveitis
Published in Ocular Immunology and Inflammation, 2022
Tat Fong Ng, Ambika Manhapra, David Cluckey, Yoona Choe, Srujan Vajram, Andrew W. Taylor
Since it is considered that tissue damage is collateral to an inflammatory response, we examined the possibility that without MC5r expression there is missing tissue sparing RPE suppression of immune cell activity. Our previous studies demonstrated that RPE suppresses phagosome maturation at an early stage, down-regulate lysosomal-associated membrane protein 1 (LAMP-1) expression needed for phagolysosome formation and activation in macrophages.11,12 Therefore, we examined the possibility that α-MSH-therapy promoted RPE recovery of its ability to govern innate immune cell activity by suppressing phagolysosome activation in macrophages. Cultures of RPE eyecups from EAU WT and MC5r(-/-) mouse eyes were collected on EAU Day 65 for the WT and Day 90 for the MC5r(-/-) mice. These mice were either untreated or treated with α-MSH. Age-matched naive mouse RPE eyecups were also collected. The conditioned media of cultured RPE-eyecups were used to treat macrophages given opsonized pHrodo-Red bioparticles to phagocytize. The phagocytized pHrodo-Red-bioparticles are weakly fluorescent before they are in an activated phagolysosome where the acidic conditions make the bioparticles fluoresce at their maximum intensity. This allows for quantifying phagolysosome activation.
Mechanisms of cellular and humoral immunity through the lens of VLP-based vaccines
Published in Expert Review of Vaccines, 2022
Hunter McFall-Boegeman, Xuefei Huang
Because most VLP-based vaccines targeting T cell responses do not attempt to directly activate T cells, attention must be paid to the cross-presentation pathway in APCs. Cross-presentation is not as simple as the name suggests. It is not a single pathway but is a combination of multiple pathways that result in the same outcome, that is, fragments of proteins of extracellular origin presented on MHC class I molecules. Figure 2 shows the complex nature of cross-presentation. The first step regardless of pathway is phagocytosis of the VLP by the APC. The phagosome then fuses with the lysosome creating a phagolysosome. Here is where the pathways diverge. There are three main cross-presentation pathways with each having minor pathways, which are still being fiercely debated in the literature[112,114–116].
The role of cells and their products in respiratory drug delivery: the past, present, and future
Published in Expert Opinion on Drug Delivery, 2020
Claire H. Masterson, Sean D. McCarthy, Daniel O’Toole, John G. Laffey
Due to their phagocytic ability and homing ability toward sites of inflammation, macrophages have been investigated as ‘Trojan horse’ cells – delivering targeted therapeutics while protecting them from immune system clearance [47]. Macrophages used for experimental drug delivery are mainly derived from immortalized cell lines such as murine J774 or RAW 264.7 [48], but they can also be isolated from tissues (tissue-resident macrophages) [49], and by differentiation of circulating monocytes [50,51]. Many cells including macrophages [49] and stem cells [52] can take up therapeutics passively without affecting cell viability or homing capacity. The macrophage microenvironment and/or the therapeutic agents themselves can be augmented to induce phagocytosis by macrophages [53] which can be exploited as a means of cell loading and has been investigated using superparamagnetic iron oxide nanoparticles [50]. Macrophage interaction with lipoplexes and nanoparticles can influence phagocytosis due to the particle’s surface charge where either positive or negative charge can enhance phagocytosis depending on the specific materials used, for example poly(lactic-co-glycolic acid) (PLGA) versus poly(acrylic acid) (PAA) respectively [48,51]. Phagocytosis of the therapeutic agent often leads to its accumulation in the phagolysosome and associated problems such as degradation or interrupted release. A clever approach to this utilized a phagocytosis-resistant ‘backpack’ for the cells which could harbor and deliver the therapeutic payload, and release it in a controlled fashion [54].