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Nanomedicines for Ocular NSAIDs: State-of-the-Art Update of the Safety on Drug Delivery
Published in Lajos P. Balogh, Nano-Enabled Medical Applications, 2020
Joana R. Campos, Joana Araújo, Elisabet Gonzalez-Mira, Maria A. Egea, Elena Sanchez-Lopez, Marta Espina, Selma B. Souto, Maria L. Garcia, Eliana B. Souto
The main products of the cyclo-oxygenase (COX) pathway are prostaglandins (PGs), probably derived from the iris ciliary body [28]. PGs cause miosis, increase in vascular permeability of the blood–ocular barriers and changes in intraocular pressure. Furthermore, they possess chemokinetic activity and can serve as mediators in both humoral and cellular phases of the inflammatory response [24, 25]. The main products of lipoxygenase (LO) pathway are leukotrienes (LT) such as LT B4 and peptidoleukotrienes. LT B4 causes aggregation of polymorphonuclear cells, exudation of plasma, translocation of calcium and stimulation of phospholipase A2 [24, 29]. Peptidoleukotrienes result in bronchoconstriction, secretion of mucus, plasma leakage from post capillary venules, vasoconstriction of arterioles and miosis.
Tumor-Associated Macrophages
Published in Gloria H. Heppner, Amy M. Fulton, Macrophages and Cancer, 2019
The role that the tumor microenvironment plays in directing the appearance and function of TAM may be complex. Thus, tumors may contribute both prochemotactic, chemokinetic, and antichemotactic factors. In addition, some of these factors seem to be relatively more or less active for different macrophage populations, e.g., activated vs. resident. CSF activities from tumors have been described in many systems, however, the in vivo role for these activities is, again, in doubt. They may, in fact, be responsible for some systemic effects such as granulocytosis without affecting TAM populations.
Overproduction of Hyaluronan in the Tumor Stroma
Published in Róza Ádány, Tumor Matrix Biology, 2017
Warren Knudson, Cheryl B. Knudson
Besides the formation of loose, hydrated extracellular avenues conducive to cell migration, it is becoming increasingly clear that high concentrations of hyaluronan also play a direct, interactive role in cell migration — a role mediated via tumor cell surface, hyaluronan-specific receptors. Some receptors are primarily involved in cell locomotion while others promote kinase-dependent chemokinetic responses within the tumor cells. Besides effects on invasive properties, correlations between the metastatic potential of tumor cells and the expression of specific isoforms of hyaluronan receptors are being found. Finally, it is also becoming understood that the natural “stop” signals invoked to terminate normal physiological invasion processes, such as occur during embryonic development, also involve the interaction of hyaluronan, hyaluronan receptors, and particular matrix hyaladherins. These stop signals may have similar effects on tumor cells during the early stages of invasion. Thus, the temporal/spatial deposition of hyaluronan, hyaluronan receptors, and matrix hyaladherins can serve as signals or matrix cues to alter cell behavior.
Herpes Simplex Conjunctivitis and Recurrent Chalazia in a Patient DOCK8 Deficiency
Published in Ocular Immunology and Inflammation, 2022
Tinh Le, Basak Can, Faruk Orge
Hyperimmunoglobulinemia E (Hyper-IgE) syndrome (HIES) is a rare hereditary immunodeficiency characterized by elevated serum IgE levels. The condition’s classical features are early-onset eczema and recurrent skin and pulmonary tract infections, typically caused by Staphylococcus aureus and Candida albicans.1,2 Various mutations, both autosomal dominant and recessive, can produce the phenotype of Hyper-IgE syndrome. Despite their different mechanisms with varied constellations of systemic manifestations, they all act by interfering with leukocyte chemokinesis and T-helper cell development.1 Heterozygous mutations in the STAT3 transcription factor gene are the most common cause of autosomal dominant (AD) cases, where skeletal and connective tissue abnormalities such as coarse facial features are frequent. Most autosomal recessive (AR) cases occur as a result of mutations in the Dedicator of Cytokinesis 8 (DOCK8) guanine nucleotide exchange factor (GEF), and clinical features of these patients include lower rates of skeletal abnormalities, higher rates of asthma and allergies, and higher rates of treatment-resistant, widespread cutaneous viral infections, often due to herpesviruses or HPV.3,4
IL-26 in asthma and COPD
Published in Expert Review of Respiratory Medicine, 2022
Eduardo I. Cardenas, Karlhans Fru Che, Jon R. Konradsen, Aihua Bao, Anders Lindén
So far, the expression of the IL-26 receptor complex in human airways has been reported in bronchial epithelial cells [35] and alveolar macrophages only [25], though it has also been identified in blood neutrophils from healthy donors [37] and in CD4+ T cells isolated from tuberculous pleural effusion [39]. Previous studies found that IL-26 induced the expression of TNFα, IL-8, and IL-10 in different human epithelial cell lines and primary keratinocytes via the IL-26 receptor complex [43,44]. Intriguingly, in vitro stimulation with IL-26 increased the transcription of pro-inflammatory mediators (e.g. TNFα, IL-1β, and IL-8) in alveolar macrophages [25] but inhibited the production of these same mediators in bronchial epithelial cells [37], all cells being of human origin. Moreover, bronchial epithelial cells responded to IL-26 stimulation by upregulating the expression of the IL-26 receptor complex and its associated transcription factors STAT1 and STAT3 [37]. In CD4+ T cells from tuberculous pleural effusion, exposure to IL-26 resulted in increased IL-22, TNFα, and IL-6 release [39]. Blood neutrophils, on the other hand, showed enhanced IL-8- and fMLP-dependent chemotaxis, reduced chemokinesis, decreased myeloperoxidase and elastase secretion, as well as downregulation of the IL-26 receptor complex, STAT1, and STAT3 in vitro in response to IL-26 [37,38]. These varied outcomes highlight the cell type- and tissue-specific effects of IL-26 (Figure 1).
Emerging growth factor receptor antagonists for ovarian cancer treatment
Published in Expert Opinion on Emerging Drugs, 2018
Luisa Bonilla, Amit Oza, Stephanie Lheureux
Normal follicle development in the ovary is in part mediated by IL-6 cytokine [108]. In the tumor, IL-6 is considered to induce tumor growth, improve chemotactic and chemokinetic cell action, and increase invasiveness [109]. In EOC, IL-6 is considered to have an autocrine effect in tumoral cells increasing proliferation pathways, like JAK/STAT, Ras/MEK/Erk and PI3K/Akt, inducing also angiogenesis [110,111]. This effect occurs primarily by IL-6 binding to its receptor, triggering the intracellular signal transduction. IL-6 levels in serum and ascitic fluid in EOC patients have been correlated with disease tumor burden. Therefore, high serum levels of IL-6 represent a poor prognostic factor for EOC. Additionally, high level of IL-6 are also predictive for low response to chemotherapy [112,113]. The role of IL-6 in EOC proliferation represents an opportunity for targeting treatment [114].