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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).
Pathophysiology of asthma
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
Eosinophils are considered key cells in asthma. Airway eosinophilia is mainly driven by IL-5, which promotes the production of eosinophils in the bone marrow and contributes to the recruitment of eosinophils through the influence of chemokines such as eotaxins 1, 2, and 3 (CCL11, CCL24, and CCL26, respectively); regulated upon activation, normal T cell expressed and secreted (RANTES); macrophage inflammatory protein (MIP)-1α; and arachidonic acid metabolites including cysteinyl leukotrienes and 5-keto eicosatetraenoic acid [36]. This type of cell increases in the bronchial mucosa after an allergic response. Its pro-inflammatory effects result in the liberation of cytokines, such as IL-3, IL-4, IL-5, and IL-13, various basic proteins, chemokines, growth factors, enzymes, and lipid mediators.
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
Allergic insult of the lung leads to a coordinated recruitment of eosinophils. Upon such insult, lung tissue produces the cytokine interleukin-5 (IL-5), along with eotaxin chemokines, which are three closely related chemokines, CCL11,52,53 CCL24,54 and CCL26,55,56 whose only known receptor (as agonists) is CCR3. Eosinophils express CCR3 and specific receptors for IL-5, and functional blockade of either the IL-5 receptor or CCR3 inhibits eosinophil accumulation in lung.57
IL-1α antibody inhibits dose-dependent exacerbation of eosinophilic inflammation by crude house-dust-mite antigen in the conjunctiva of an atopic keratoconjunctivitis mouse model
Published in Current Eye Research, 2021
Yukiko Shiraki, Jun Shoji, Noriko Inada, Akiko Tomioka, Satoru Yamagami
Atopic keratoconjunctivitis (AKC), first reported by Hogan in 1953,1 is a bilateral, chronic allergic disorder that develops in the face and eyelid skin of patients with atopic dermatitis. The primary symptom of AKC is seasonal or perennial ocular itching; the representative objective findings in the ocular surface include blepharitis, papillary or giant papillary formation in the upper tarsal conjunctiva, conjunctival hyperemia and swelling, subepithelial fibrosis of the conjunctiva, superficial punctate keratitis, and shield ulcer.2 The characteristic histological findings of AKC are severe subepithelial infiltration of eosinophils and lymphocytes, pseudotubule formation, and frank granuloma formation in the conjunctiva.3 Moreover, the level of eosinophil cationic protein, an eosinophil granule protein, significantly increases in patients with AKC in compared with that in normal subjects, in the tear test.4 Previously, we reported that the mRNA level of CCL24/eotaxin-2 significantly correlated with the clinical scores in patients with AKC or vernal keratoconjunctivitis (VKC).5 We also demonstrated that CCL24/eotaxin-2 is a suitable ocular biomarker for allergic inflammation in AKC and VKC. Specifically, type 2 inflammation, which is mainly dependent on the helper T cell type 2 (Th2) response, is considered to be associated with allergic inflammation in AKC, similar to that of atopic dermatitis. However, the pathophysiology of type 2 inflammation caused by the innate immune response in AKC is not fully understood.
Diagnosis and treatment of non-allergic rhinitis: focus on immunologic mechanisms
Published in Expert Review of Clinical Immunology, 2021
Yifan Meng, Chengshuo Wang, Luo Zhang
Other mediators have also been shown to be involved in the pathogenesis of NARES. The levels of IL-17, a cytokine responsible for neutrophilic infiltration and remodeling process, has also been found to be elevated in nasal secretions from patients with NARES, compared to patients with persistent allergic rhinitis and control subjects [18]. Similarly, Corso et.al [23] have found higher levels of eotaxin-3 (CCL26) and eotaxin-2 (CCL24) in nasal secretions of NARES patients compared to controls, suggesting that CCL26 and CCL24 may play a role in pathogenesis of NARES. Powe et.al [24] investigated the mechanism underlying the IgE-independent hypersensitivity response in NARES, and demonstrated that immunoglobulin (Ig) free light chains, involved in antigen-induced mast cell activation, were significantly increased in nasal secretion and serum of NARES patients compared to control subjects [24].
Plasma pro- and anti-inflammatory cytokines may relate to cocaine use, cognitive functioning, and depressive symptoms in cocaine use disorder
Published in The American Journal of Drug and Alcohol Abuse, 2021
Sydney N. Stamatovich, Paula Lopez-Gamundi, Robert Suchting, Gabriela D. Colpo, Consuelo Walss-Bass, Scott D. Lane, Joy M. Schmitz, Margaret C. Wardle
For cognition, two predominantly pro-inflammatory cytokines were selected: Eotaxin-2 CCL24 and TWEAK. These cytokines related to better overall cognitive performance, again inconsistent with our original hypothesis. Eotaxin-2 CCL24 was the most highly selected cytokine overall, being identified in >80% of models. Eotaxin-2 CCL24 is another member of the CC chemokine family, and is associated with aspirin-exaggerated respiratory disease (AERD) (69). A small number of studies suggest that it is also associated with psychiatric disorders. In particular, lower levels of Eotaxin-2 CCL24 are associated with bipolar disorder, although levels are elevated in individuals with major depressive disorder (70,71). Research on the broader Eotaxin family suggests that this family plays a role in cognition and neurodegeneration. Eotaxin-1 CCL11 and CCL26 are elevated in Alzheimer’s and Huntington’s diseases, and as noted above, Eotaxin-1 CCL11 related to poorer cognition in methamphetamine users; however, there are no prior findings suggesting that Eotaxin-2 CLL24 has the same impact (72,73). TWEAK is part of the pro-inflammatory TNF superfamily and plays a significant role in apoptosis, elevation of B cells, transplant rejection, and cell proliferation. Lower levels of TWEAK were found in crack cocaine-dependent women compared to a healthy control group (74). Thus, the relationship between higher levels of TWEAK and better cognitive performance on the Shipley-2 is more in line with previous research, despite its status as a pro-inflammatory marker.