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Infection and Inflammation
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Erik H. J. G. Aarntzen, Andor W. J. M. Glaudemans
In particular, macrophages release soluble factors, for example, prostaglandins, leukotrienes, and platelet-activation factor, or chemokines, which facilitate the recruitment of other immune cells [5–7]. For example, tumour-necrosis factor α (TNFα) is an activator of endothelial cells; interleukin-8 (CXCL8) is involved in the recruitment of neutrophils to the site of infection, and interleukin-1β (IL-1β) and interleukin-6 (IL-6) induce systemic acute-phase responses in the liver. Antibody-antigen complexes and surface molecules on pathogens can induce the activation of other, non-eukaryotic, components of the immune system; the complement system, and platelets [8, 9]. The complement system consists of plasma proteins that react to mark pathogens for phagocytosis, a process called opsonization, and help exaggerate immune response.
Dermal filler complications and management
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
The complement system is comprised of approximately thirty proteins which are synthesised by the liver and are permanently in circulation in blood plasma. When complement proteins are triggered by microbial antigens, a cascade of events is initiated with the intention of destroying pathogens through phagocytosis, cytolysis and inflammation. Phagocytosis is triggered via a process called opsonisation, where opsonin proteins are used to mark infected or dying cells to be phagocytosed. Cytolysis occurs through the formation of the membrane attack complex (MAC) which effectively punches a hole within the plasma membrane of bacteria, causing them to rupture due to an inflow of extracellular fluid. Finally, inflammation is stimulated by the binding of complement proteins to mast cells to encourage them to secrete histamine which increases blood vessel permeability to allow cells of the immune system to extravasate and reach the target area.
Engineered Nanoparticles for Drug Delivery in Cancer Therapy *
Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Tianmeng Sun, Yu Shrike Zhang, Pang Bo, Dong Choon Hyun, Miaoxin Yang, Younan Xia
When nanoparticles enter the plasma, opsonization (i.e., the adsorption of serum proteins) will occur immediately on their surfaces [5, 160a]. Through opsonization, foreign organisms or particles will be coated with nonspecific proteins known as opsonins to generate a corona and make the particles more visible to the phagocytic cells in the MPS. Opsonins typically contain complement proteins and immunoglobins (usually IgG) along with albumins, fibronectins, fibrinogens, and apolipoproteins [194]. Studies have shown that the corona has a layered architecture. It starts with an inner layer of proteins that strongly adsorb onto the surface, with Kd 10−6 to 10−8 m, to form the hard corona, which is then surrounded by a layer of soft corona formed by weak interactions [169, 195]. The primary driving forces for opsonization are based on hydrophobic and electrostatic interactions, together with entropic and conformational changes for the adsorbed proteins [196]. Depending on the charge and hydrophobicity of the nanoparticles, opsonization can occur within minutes. Experimental results suggest that a charged surface tends to be covered by proteins more rapidly than their counterparts with a neutral surface [160a].
Biodistribution and targeting properties of iron oxide nanoparticles for treatments of cancer and iron anemia disease
Published in Nanotoxicology, 2019
Although the different parameters that influence iron oxide nanoparticle biodistribution are interdependent the following features have been reported in some specific cases for these parameters:IONP size. It that has an impact on: (i) t1/2 values, i.e. t1/2 increases with decreasing IONP sizes, (ii), the route of elimination, i.e. IONP > 200 nm are degraded in spleen, 10 nm < IONP < 200 nm are eliminated in liver and spleen, while IONP < 10 nm are excreted through kidney.IONP Hydrophobic/Hydrophilic properties. Hydrophobic IONP yields a shorter circulation time than hydrophilic ones.IONP surface charge. Positively charged IONP have a faster clearance than negatively or neutrally charged ones.IONP coating. IONP specific coating, such as PEG, can prevent nanoparticle capture by macrophages.IONP administration route. It determines in which organ IONP distribute and how they are eliminated.Opsonization. When IONP are opsonized or when their quantity administered increases, it can lead to an increase in t1/2 values.
Applying lessons from human papillomavirus vaccines to the development of vaccines against Chlamydia trachomatis
Published in Expert Review of Vaccines, 2018
Kathryn M. Frietze, Rebeccah Lijek, Bryce Chackerian
Antibody could also prevent Ct infection by serving as an opsonin, thereby enhancing clearance of extracellular bacteria by phagocytes. A recent report indicates that IFN-γ-stimulated neutrophils can kill Ct in vitro, and this killing requires Ct-specific serum [41]. This suggests that vaccine-induced antibody against Ct might also increase opsonophagocytic killing of Ct by neutrophils and macrophages. Conversely, there are also reports that Ct can infect cultured macrophages in vitro [42–44]. Whether or not these phenotypes hold true in vivo remains to be determined. It will be important to fully investigate the activity of any antibodies elicited by vaccine candidates for their opsonization versus enhanced infection capabilities in vitro and in vivo.
Complement inhibitor factor H expressed by breast cancer cells differentiates CD14+ human monocytes into immunosuppressive macrophages
Published in OncoImmunology, 2020
Karolina I. Smolag, Christine M. Mueni, Karin Leandersson, Karin Jirström, Catharina Hagerling, Matthias Mörgelin, Paul N. Barlow, Myriam Martin, Anna M. Blom
Complement inhibitor factor H (FH) is mainly expressed in the liver, but also extrahepatically by various cell types, including ovarian14 and lung15 cancer cell lines. FH has been shown to affect myeloid cell functions not related to complement, including chemotactic effects on monocytes,16 stimulation of prostaglandin E from perinatal macrophages17 and restraining mononuclear phagocytes at the site of inflammation.18 Previously, we revealed that opsonization with FH increased the clearance of apoptotic cell remnants and skewed the resultant cytokine production by phagocytes to an anti-inflammatory profile.19