China
Africa
Explore chapters and articles related to this topic
How to Assess Your Risk Using CHD Scoring Tests
Published in Mark C Houston, The Truth About Heart Disease, 2023
Biomarkers:MCP-3: immune cell direction and activity.sFas: prevents apoptosis (cell death).Fas ligand: initiates cell recycling and death.Eotaxin: activates immune cells in areas of injury.CTACK: helps to clean up damaged cells.IL-16: recruits and activates immune cells and indicates inflammation.HGF: stimulates tissue repair.
Vasculitides
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Ivy M. Obonyo, Virginia A. Jones, Kayla A. Clark, Maria M. Tsoukas
Laboratory studies: Histologic study will show eosinophilia in the tissues (>10%), disseminated small vessel vasculitis, extravascular granulomatous change, and fibrinoid necrosis (Figure 13.11). When active, C-reactive protein (CRP) and ESR may be elevated. IgE is also elevated in patients with EGPA, but this is not specific. Elevated IgG4 levels are more specific and should be measured. Up to 90% of EGPA patients are positive for p-ANCA, but this is not diagnostic. Eotaxin-3, a chemokine that attracts eosinophils, is both sensitive and specific to EGPA when active.
Eosinophil–Epithelial Interactions and Transepithelial Migration
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Mary K. Schroth, James M. Stark, Julie B. Sedgwick, William W. Busse
Eotaxin is a relatively new C-C chemokine identified in guinea pig lungs following an aerosol allergen challenge (62,63). When injected into the lungs or skin, eotaxin induces the selective recruitment of eosinophils (62,63). High levels of constitutive eotaxin mRNA have been identified in guinea pig lungs and these are increased in response to allergen during the late-phase response (5). Human eotaxin has been identified and cloned; it has the same receptor as RANTES and macrophage chemotactic protein-3 (61). Finally, human eotaxin has recently been identified as an early response gene in cytokine-stimulated epithelial and endothelial cells (158). Stimulation of the epithelial cell line, BEAS-2B, with IL-1β or TNF-α yields a marked increase in eotaxin mRNA.
What place will tezepelumab hold in the treatment paradigm in chronic rhinosinusitis?
Published in Expert Review of Clinical Immunology, 2023
Valentin Favier, Jérémy Charriot, Louis Crampette, Arnaud Bourdin, Engi Ahmed
T2-polyps have been shown to be mainly composed of monotonous p63-expressing basal cells associated to a loss of the other classical epithelial subtypes notably secretory and ciliated cells [5]. Single cell RNA sequencing of NP highlighted an impairment in the differentiation ability of basal cells that accumulate at this early ontogenic state (‘basal cell hyperplasia’). Basal cells in eosinophilic CRSwNP showed the highest expression of proinflammatory genes, especially those linked to type 2 inflammation, including the nitric oxide synthase (NOS2), that may be linked to high exhaled nitric oxide (FeNO) levels, TSLP, IL-4/13-induced genes, chemokines such as eotaxin-3, CLC (Charcot-Leyden crystal), and protease inhibitors such as cystatins. Eotaxin 3 is a potent chemoattractant for eosinophils through the binding to the cell surface chemokine receptor CCR3.
Cyclo-VEGI inhibits bronchial artery remodeling in a murine model of chronic asthma
Published in Experimental Lung Research, 2021
Kyung Hoon Kim, Jung Hur, Hwa Young Lee, Eung Gu Lee, Sook Young Lee
Elastin stimulation enhanced fibroblast proliferation and eotaxin production (Figure 6). Eotaxin is a CC chemokine and a potent chemoattractant for eosinophils. Eotaxin is a key factor in the migration of eosinophils from bone marrow and stimulates the extravasation of eosinophils from peribronchial arteries into peribronchial tissues by acting on eosinophils.29,30 Furthermore, eotaxin is a key mediator that participates in the activation and prolonged survival of eosinophils.4 In our study, elastin stimulation enhanced fibroblast proliferation and eotaxin production, as shown in Figure 6. Moreover, production of TGF-β1 by fibroblasts decreased upon elastin stimulation. TGF-β1 can inhibit the activation of eosinophils.31 We also demonstrated that cyclo-VEGI inhibited elastin-stimulated fibroblast proliferation and reduced eotaxin secretion in fibroblasts through in vitro experiments. These results, together with the results of the in vivo study, showed that the effect of cyclo-VEGI on the reduction of elastin deposition in perivascular areas resulted in decreased eotaxin levels and that this effect could be related to perivascular remodeling by inhibiting extravasation and recruitment of eosinophils. Therefore, we presumed that vascular remodeling was responsible for the aggravated eosinophilic airway inflammation, which was suppressed by cyclo-VEGI according to our experimental results.
Eosinophilic pneumonia: a case of daptomycin induced lung injury
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Vaishnavi Raman, Isha Chaudhary, Sean Shieh
To effectively assess this condition, it is important to understand the pathophysiology. One study proposed that the detection of antigens by alveolar macrophages leads to the recruitment of T-helper 2 lymphocytes and the release of interleukin 5. The function of interleukin 5 is to induce the production of eosinophils and migration to the lung. Eotaxin, an eosinophil chemoattractant, is produced by alveolar macrophages and other cells in the lungs. This substance further induces an accumulation of eosinophils. It is hypothesized that daptomycin is retained in the pulmonary surfactant and when concentrations become high enough, it can lead to injury of the surrounding tissues. This injury will then activate alveolar macrophages and initiate the process of eosinophil accumulation [12].