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Fibroblast and Immune Cell Cross Talk in Cardiac Repair
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Stelios Psarras, Georgina Xanthou
There is evidence that neutrophil chemoattractants are overexpressed by cardiac fibroblasts in MI. Indeed, in mice lacking 11β-hydroxysteroid dehydrogenase type 1, CXCL2 and CXCL5 overexpression by cardiac fibroblasts was accompanied by increased neutrophilic inflammation (Figure 5.1), which was reversed by administration of corticosterone (38). Moreover, cardiac fibroblasts produce eotaxins (CCL11 and CCL24) and recruit eosinophils (Figure 5.1) in certain myocarditis conditions (39).
Anti-Inflammatory Properties of Bioactive Compounds from Medicinal Plants
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Muhammad Imran, Abdur Rauf, Anees Ahmed Khalil, Saud Bawazeer, Seema Patel, Zafar Ali Shah
In the BALF, marked inhibition in elevated inflammatory cells and cytokine (Th2) was noticed due to application of rosmarinic acid. It also decreased ova-specific IgE and total IgE contents and AHR (ameliorated airway hyper-responsiveness) and reduced the content of mucus hypersecretion and inflammatory cells in the airway. Additionally, rosemarinic acid could be facilitated due to inhibition of JNK, ERk and phosphorylation of p38 along with NF-κB (nuclear factor-κB) activation. Moreover, in lung tissue, pre-treatment of RA caused significant decline in expression of CCL11, AMCase, Ym2, CCR3, and E-selection mRNA [43].
mTBI in the Military and Contact Sports
Published in Mark A. Mentzer, Mild Traumatic Brain Injury, 2020
Fortunately for the sport and its players, for a participant and those considering participation, and for the benefit of many others, including military patients with head injury, Dr. Omalu has continued his involvement in the field. Along with his colleagues he recently helped identify a chemical radiologic marker called FDDNP used in conjunction with PET scanning to identify the presence of tau and amyloid proteins (Omalu et al., 2018). Omalu also identified a specific gene allele in the player brains he examined, suggesting a possible genetic predisposition to CTE. Dr. McKee also continues to support research in the field as director of the brain bank at BU. She and her colleagues are investigating the cytokine CCL11 in CTE and the prion-like spread of CTE tau.
Targeting interleukin 4 and interleukin 13: a novel therapeutic approach in bullous pemphigoid
Published in Annals of Medicine, 2023
Fangyuan Chen, Yiman Wang, Xinyi Chen, Nan Yang, Li Li
Eosinophilia is a typical pathological feature of BP. The numbers of eosinophils and secretory granules (e.g. eosinophil cationic protein) in serum are reportedly correlated with the severity of BP [52,53]. Eosinophils can promote the pathogenesis of blistering in BP by releasing proteolytic enzymes and producing extracellular traps [35,54]. Pruritus in BP could last for months or remain the only symptom, which is difficult to control [55]. The mechanism underlying the onset of pruritus in BP may include multiple mediators, such as cytokines, chemokines, proteases, and associated receptors [56]. The study by Hashimoto et al. indicated that eosinophil is related to pruritus severity of BP [56], presumably because of chemokines activated by eosinophils. A meta-analysis revealed that numerous chemokines were elevated in BP. The levels of CCL11 (eotaxin 1), CCL17, and tumor necrosis factor-α were elevated in blister fluid, whereas CCL26 (eotaxin 3) was elevated in serum [57]. CCL11 and CCL26 are important chemokines that mediate eosinophil infiltration and degranulation. Additionally, IL-31, a Th2 cytokine primarily expressed by eosinophils in BP [58], may also contribute to pruritus in BP.
Factors associated with the activity and severity of bullous pemphigoid: a review
Published in Annals of Medicine, 2020
Yangchun Liu, Yiman Wang, Xinyi Chen, Hongzhong Jin, Li Li
The level of chemokines is determined using ELISA kits. Eotaxin-1 (CCL11) and eotaxin-3 (CCL26) belong to the eotaxin subfamily of CC-chemokines, and their expression is up-regulated in the serum and blister fluid of BP patients. CCL26 is also expressed strongly in the lesions of BP patients. CCL11 and CCL26 are associated significantly with eosinophil activation, especially serum levels of CCL26, which has a close correlation with eosinophil numbers in peripheral blood. Hence, CCL26 levels could be useful for assessing BP activity, and have a role in BP development. Blockade of CCL26 function could provide a novel target for treating BP [30]. CCL11 can bind to the CCR3 expressed on eosinophils and induce eosinophil chemotaxis [31]. In addition, several observations presented that levels of eotaxin, IL-5 and CCR3 were increased in the blister fluid as well as the lesional and peri-lesional skin of BP patients. These markers also have a significant correlation with the number of dermal-infiltrating eosinophils [22,32]. There had been a pilot phase 2a study proving that bertilimumab, an anti-eotaxin-1 antibody, was safe and efficacious in the treatment of BP. This finding provided a novel target for treating BP, however, a larger controlled trial would be expected [33].
Blood biomarkers for assessment of mild traumatic brain injury and chronic traumatic encephalopathy
Published in Biomarkers, 2020
Matthew I. Hiskens, Anthony G. Schneiders, Mariana Angoa-Pérez, Rebecca K. Vella, Andrew S. Fenning
CCL11 is a chemokine found throughout the body. It appears to have unique function in the CNS, with CSF and plasma levels increasing in mice and humans as part of normal aging (Villeda et al.2011). In healthy individuals, CCL11 is generated in the choroid plexus (Baruch et al.2013). However, following TBI, microglia and astrocytes may also contribute to CCL11 release (Kovac et al.2011, Parajuli et al.2015). CCL11 increase in mice was related cognitive and memory impairment and a reduction in neurogenesis (Villeda et al.2011). CNS inflammation stimulates CCL11 release, which then triggers an increase in microglial generation of ROS and excitotoxic pathways of synaptic dysfunction and neuronal death (Parajuli et al.2015). These pathways may contribute to the tau pathology seen in CTE and the associated clinical symptomology (Cherry et al.2016). As with other inflammation of the CNS, the release of CCL11 is intended to provide protection and repair in states of trauma. However, excessive trauma, or repetitive trauma as is often seen in the aetiology of CTE, leads to chronic release of CCL11 and its neurodegenerative cascade (Cherry et al.2017). Through these mechanisms, CCL11 affects neurons and displays its characteristic impaired cognition.