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Acoustically Reflective Nanoparticles for Tumor Diagnosis
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
R. G. Aswathy, D. Sakthi Kumar
molecular imaging of thrombus size reduction in carotid arteries of mice. In another study, MBs specific for VCAM-1- and P-selectin-displayed enhanced sensitivity for detecting atherogenic phenotype before the appearance of disruptive atherosclerotic lesions [38]. It was demonstrated contrast that enhanced US and VCAM-1-targeted MB could be used to observe vascular inflammation in pigs. MB conjugated to recombinant P-selectin glycoprotein ligand-1 (PSGL-1) analog presented superior binding to the endothelium post intramuscular administration of endotoxin than sialyl Lewis X-contained or antibody-coupled MB [39].
Intestinal macrophages in defense of the mucosa
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Lesley E. Smythies, Phillip D. Smith
In studies of macrophage accumulation in inflamed gastrointestinal mucosa, immunohistochemical analysis has shown that the endothelial cells lining small blood vessels in the mucosa of patients with Crohn's disease display high levels of CD34, a ligand that promotes the rolling of L-selectin+ monocytes in high endothelial venules. More recently, antibody blocking studies have revealed that P-selectin glycoprotein ligand-1, P-selectin, and vascular cell adhesion molecule-1 (VCAM-1) promote CD14+ monocyte rolling and adherence in the intestinal mucosa, particularly ileal mucosa, in a mouse model of spontaneous ileitis. Increased levels of intercellular adhesion molecule-1 (ICAM-1) and CD31, which facilitate the transendothelial migration of monocytes, are also present in Crohn's disease lesions. Thus, endothelial cells in mucosal vessels express molecules that promote the rolling, adherence, and subsequent transendothelial migration of circulating blood monocytes into inflamed gastrointestinal mucosa. In addition, recruitment factors, including CCL2 and CCL4, which selectively induce monocyte transendothelial migration and accumulation, may be released in inflamed and/or infected mucosa, enhancing the migration of monocytes into the mucosa. The interdiction of such recruitment is an attractive therapeutic strategy, but localization of such therapy to inflammatory sites will be difficult to achieve.
Lymphocyte homing and immunology of extranodal lymphoid tissues
Published in Franco Cavalli, Harald Stein, Emanuele Zucca, Extranodal Lymphomas, 2008
Mariagrazia Uguccioni, James J Campbell, Katrin Kuscher, Marshall E Kadin
The intestinal lamina propria (LP) contains numerous previously activated/memory CD4+ T-cells involved in intestinal immunity and the induction and maintenance of chronic intestinal inflammation.41 T-cell entry into the intestinal mucosa is mediated by distinct sets of cell adhesion molecules expressed on the T-cell and intestinal microvascular endothelial surface. Interaction between the gut-associated integrin α4β7, on the T cell surface, with its ligand MAdCAM-1, on intestinal microvascular endothelium cells, is important for T-cell entry into the LP.42–44 Moreover, antibody neutralization studies suggest a role for P-selectin and P-selectin glycoprotein ligand 1 (PSGL-1) in effector CD4+ T-cell entry to this site. The chemokine receptor CCR9 is required for efficient effector CD8+ T-cell localization to the small intestinal epithelium.40,45
Controlling in and out – the future of interfering with immune cell trafficking in inflammatory bowel disease
Published in Expert Review of Clinical Immunology, 2023
Sebastian Zundler, Lisa Lou Schulze, Markus F. Neurath
In order to slow down the leukocytes in the blood stream and to bring them in closer contact to the endothelium and tissue-derived stimuli that mediate arrest, rolling along the endothelial wall is induced by the interaction of P-, E-, and/or L-selectin with their respective ligands. These molecules are all expressed either on the leukocyte surface or the endothelium [15–18]. While P-selectin glycoprotein ligand 1 (PSGL1) can serve as a ligand for each of the selectins, E-selectin ligand-1 (ESL1) and CD44 bind E-selectin and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) interacts with L-selectin. These interactions create loose contacts resulting in a rolling behavior of the immune cells along the vessel wall [14,15,19,20]. In addition, rolling behavior can also be achieved by weak interactions of the integrins α4β7 and α4β1 with their respective ligands MAdCAM-1 and vascular cell adhesion molecule 1 (VCAM-1) [14,21,22].
Inflammation-targeted cannabidiol-loaded nanomicelles for enhanced oral mucositis treatment
Published in Drug Delivery, 2022
Yingke Liu, Xingying Qi, Yashi Wang, Man Li, Quan Yuan, Zhihe Zhao
To further evaluate the inflammation degree, the presence of Ly6G cells, which include polymorphonuclear neutrophils or polymorphonuclear myeloid-derived suppressor cells (MDSCs), was assessed by Ly6G staining. Normal tongue tissue served as control, where no Ly6G cell infiltration was observed (Supplementary Figure S5). Compared to PBS and free CBD, CBD/FD nanomicelles significantly reduced Ly6G cell infiltration, exhibiting an improved anti-inflammatory effect. (Figure 6(A)). The interaction of P-selectin glycoprotein ligand 1 (PSGL-1) expressed on Ly6G + cells and P-selectin expressed on vascular endothelial cells mediated the process of cell infiltration. Therefore, we speculate that the reduced infiltration of Ly6G cells is partly due to the ability of fucoidan competitively bind to P-selectin. It is analogous to how low-molecular-weight heparin can competitively bind P-selectin and thereby inhibits the recruitment of MDSCs (Stadtmann et al., 2013; Long et al., 2020).
Role of extracellular vesicles in severe pneumonia and sepsis
Published in Expert Opinion on Biological Therapy, 2022
Wonjung Hwang, Masaru Shimizu, Jae-Woo Lee
PEVs acts on leukocytes and activated endothelial cells at the site of vascular injury. These EVs contribute to the activation of the immune system by facilitating cell aggregation, cell-to-cell interactions, and the release of cytokines[33–35]. PEVs induce platelet aggregation and enhances leukocytes recruitment via chemokine release as well as the recruitment of other immune cells such as monocytes, T- and B-lymphocytes, and natural killer cells. The binding of PEVs to P-selectin and P-selectin glycoprotein ligand 1 enhances leukocyte–leukocyte interactions and monocyte-endothelial cell interactions[36,37]. PEVs increase the expression of cyclooxygenase-2 in monocytes, which converts AA into prostacyclin. Prostacyclin causes vasodilation that allows inflammatory cells to reach the site of infection[38]. PEVs can stimulate production of pro-inflammatory cytokines including IL-1, IL-6, IL-8, TNF-α, and monocyte chemoattractant protein 1 (MCP-1). These cytokines can activate inflammatory cells to release additional EVs, further aggravating the injury[39]. For example, in transfusion-related ALI, a high concentration of the ligand CD40L/CD154 on PEVs were correlated with antigen-specific adverse reactions[40].