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Anti-Inflammatory Compounds Derived from Marine Macroalgae
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Snezana Agatonovic-Kustrin, David W. Morton
Their mechanism of anti-inflammatory activity is believed to be similar to the action of heparins (Colliec-Jouault et al. 2012). Fucoidans extracted from different sources such as Fucus vesiculosus and Laminaria japonica, down-regulate the NF-қB signaling pathway and reduce the levels of several pro-inflammatory cytokines such as IL-6 and TNF-α and matrix metalloproteinases (MMPs) (Fernando et al. 2017). The adhesion of leukocytes to vascular endothelium is a hallmark of the inflammatory process. Fucoidans interfere with P- (platelet) and L- (leukocyte) selectins, cell adhesion molecules essential in the recruitment process. Selectins play important roles in leukocyte trafficking to the sites of inflammation. The rolling of leukocytes along the endothelium is mediated by selectins. Thus, fucoidans prevent leukocyte rolling on the endothelium before their adhesion and extravasation from circulation into the inflamed site (Carvalho et al. 2014). The anti-inflammatory effect of fucoidans is also attributed to the suppression of inducible iNOS expression.
Lymphocyte trafficking from inductive sites to effector sites
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Valerie Verhasselt, William Agace, Oliver Pabst, Andrew Stagg
Selectins are glycoproteins of the C-type lectin group that bind to specific carbohydrate determinants on selectin ligands. Mammals express three types of selectins: L-selectin, P-selectin, and E-selectin. L-selectin is expressed by many types of immune cells and interacts with ligands expressed by vascular endothelial cells. Conversely, E- and P-selectins are expressed by endothelial cells, and the interacting carbohydrate selectin ligands can be expressed by immune cells. Selectin ligands comprise a heterogeneous group of molecules that frequently, but not exclusively, carry the sulfated tetrasaccharide sialyl-Lewisx. Thus, the generation of functional selectin ligands depends on the posttranslational modification of proteins by glycosyltransferases. Selectins bind their ligands with low affinity, facilitating the capture of immune cells freely flowing in the blood and resulting in their rolling along the vascular endothelium.
Regulation of Eosinophil Function by P-Selectin
Published in Gerald J. Gleich, A. Barry Kay, Eosinophils in Allergy and Inflammation, 2019
Mathew A. Vadas, C. M. Lucas, J. R. Gamble, Angel F. Lopez, M. P. Skinner, M. C. Berndt
P-selectin appears to be a physiologically relevant molecule that is expressed on endothelial cell surfaces after treatment with thrombin or histamine (10) and on platelets after activation (11). P-selectin is also found in the plasma of normal individuals (5). We found that eosinophils adhere strongly to purified P-selectin (Fig. 1) or CHO cells expressing recombinant P-selectin (Fig. 2) and that this adhesion is not associated with spreading or polarization (Figs. 3 and 4) normally associated with eosinophil activation. The adhesion was inhibitable by a polyclonal antibody against P-selectin (data not shown). In comparison to cells adherent to extracellular matrix proteins, eosinophils adherent to P-selectin were deficient in generation. Fluid-phase P-selectin also inhibited eosinophil activation even after adhesion to fibrinogen (data not shown). This suggests that P-selectin signals cells and interrupts the normal activation process. Similar inhibitory effect of fluid-phase P-selectin was observed on degranulation in response to phorbol myristate acetate but not Ig Sepharose (Fig. 6), suggesting that P-selectin does not interrupt all activation pathways. This was supported by the lack of effect of P-selectin on antibody-dependent cytotoxicity (Fig. 7).
Recurrence of acute chest syndrome post stopping Crizanlizumab, the dilemma of stopping vs continuation in patient with sickle cell disease: case report
Published in Hematology, 2023
Mohammad S. Afana, Mohammad Abu-Tineh, Awni Alshurafa, Ahmed K. Yasin, Khalid Ahmed, Mohammed Abdulgayoom, Mohamed A. Yassin
Acute chest syndrome (ACS) one of the most common causes of death in SCD is defined by the presence of new chest infiltrate on imaging with respiratory symptoms and/or fever [1,8]. Three major causes have been proposed in ACS pathophysiology: pulmonary infection, bone marrow fat embolization, and pulmonary intravascular sequestration of sickled erythrocytes [9]. After VOC, ACS is the second most common cause of hospitalizations [1]. The Underlying pathophysiology of SCD complications is complex [10]. One of these involves P-selectin; an adhesion molecule found in platelets and endothelial cells. It is activated in response to inflammation and trauma. In SCD P-Selectin upregulation contributes to VOC by the adhesion of sickle red blood cells and leukocytes to the endothelial cells [11].
Therapeutic drugs and drug delivery systems targeting stromal cells for cancer therapy: a review
Published in Journal of Drug Targeting, 2020
Zhaohuan Li, Zengjuan Zheng, Chenglei Li, Zhipeng Li, Jingliang Wu, Bo Zhang
Selectins, including L-selectin, E-selectin and P-selectin, are type I transmembrane protein [63]. L-selectin is only expressed on the surface of leukocytes. Leukocyte-mediated multiple inflammatory reactions that promote tumour growth and metastasis. E-selectin is expressed on the endothelial cells, which mediates the binding of the leukocytes with the endothelial cells. The ligand of E-selectin can enhance the adhesion between tumour cells and endothelial cells, which is beneficial to the metastasis of tumour cells [64]. P-selectin is mainly expressed on platelets and endothelial cells. P-selectin not only promotes the interaction between endothelial cells and platelet cells through microthrombus, but also promotes the combination of platelets with tumour cells, which can accelerate the progress of the tumour. Because the ligands of selectins are expressed on the surface of tumour cells, the interaction between tumour cells and endothelial cells can promote the adhesion and metastasis of tumour cells [65].
Lung cancer: active therapeutic targeting and inhalational nanoproduct design
Published in Expert Opinion on Drug Delivery, 2018
Nasser Alhajj, Chin Fei Chee, Tin Wui Wong, Noorsaadah Abd Rahman, Noor Hayaty Abu Kasim, Paolo Colombo
Selectin receptor is a family of calcium-dependent receptors including three different members, namely, L-, E-, and P-selectins. Selectin receptors regulate leukocyte migration to inflammation sites by controlling its adhesion to vascular endothelium [52]. E-selectin receptor facilitates leukocyte arrest and extravasation to sites of injury by recognizing ligands such as sialyl Lewis X-type structure and related oligosaccharides associated with both glycolipids and glycoproteins on their surfaces [53]. In a similar way, E-selectin receptor has been reported to promote lung tumor cells attachment onto endothelium and is responsible for metastasis [54–56]. P-selectin receptors are over-expressed in lung adenocarcinoma tissues, and to a lesser extent in para-cancerous and distant tissues [57].