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Genomic organization, annotation, and ligand-receptor inferences of chicken chemokines and chemokine receptor genes based on comparative genomics
Jixin Wang, David L Adelson, Ahmet Yilmaz, Sing-Hoi Sze, Yuan Jin, James J Zhu
BMC Genomics , 2005, DOI: 10.1186/1471-2164-6-45
Abstract: Twenty-three chemokine and 14 chemokine receptor genes were identified in the chicken genome. All of the chicken chemokines contained a conserved CC, CXC, CX3C, or XC motif, whereas all the chemokine receptors had seven conserved transmembrane helices, four extracellular domains with a conserved cysteine, and a conserved DRYLAIV sequence in the second intracellular domain. The number of coding exons in these genes and the syntenies are highly conserved between human, mouse, and chicken although the amino acid sequence homologies are generally low between mammalian and chicken chemokines. Chicken genes were named with the systematic nomenclature used in humans and mice based on phylogeny, synteny, and sequence homology.The independent nomenclature of chicken chemokines and chemokine receptors suggests that the chicken may have ligand-receptor pairings similar to mammals. All identified chicken chemokines and their cognate receptors were identified in the chicken genome except CCR9, whose ligand was not identified in this study. The organization of these genes suggests that there were a substantial number of these genes present before divergence between aves and mammals and more gene duplications of CC, CXC, CCR, and CXCR subfamilies in mammals than in aves after the divergence.Chemokines are a family of small chemoattrative peptides that were originally recognized to be involved in host defense as regulators of leukocyte trafficking, but more recently have also been shown to have roles in organogenesis, hematopoiesis, and neuronal communication [1]. Their cognate receptors belong to the Class A subfamily of G-protein coupled receptor superfamily [2]. Chemokines are believed to have originated from gene duplications and these genes underwent selection during recent evolutionary time [3]. All chemokines have a characteristic cysteine motif. Similarly, chemokine receptors may also be derived from a common ancestor through gene duplications. All chemokine receptors share
Differential signaling mechanisms regulate expression of CC chemokine receptor-2 during monocyte maturation
Roderick J Phillips, Marin Lutz, Brett Premack
Journal of Inflammation , 2005, DOI: 10.1186/1476-9255-2-14
Abstract: We have used freshly isolated human monocytes and the model human monocyte cell line, THP-1, to investigate changes in the expression of a panel of monocyte and macrophage markers during monocyte differentiation. We have examined these changes by RT-PCR and FACS analysis. Furthermore, we cloned the CCR2 promoter and analyzed specific changes in transcriptional activation of CCR2 during monocyte maturation.The CC chemokine receptor 2 (CCR2) is rapidly downregulated as monocytes move down the macrophage differentiation pathway while other related chemokine receptors are not. Using a variety of biochemical and transcriptional analyses in the human THP-1 monocyte model system, we show that both monocytes and THP-1 cells express high levels of CCR2, whereas THP-1 derived macrophages fail to express detectable CCR2 mRNA or protein. We further demonstrate that multiple signaling pathways activated by IFN-γ and M-CSF, or by protein kinase C and cytoplasmic calcium can mediate the downregulation of CCR2 but not CCR1.During monocyte-to-macrophage differentiation CCR2, but not CCR1, is downregulated and this regulation occurs at the level of transcription through upstream 5' regulatory elements.Chemokines are a superfamily of small (8–10 kDa) proteins, which coordinate cellular responses to inflammation, insult or injury [1-4]. They also play a pivotal role in the regulation of leukocyte trafficking and extravasation through the luminal surface of endothelial cells into sites of tissue inflammation. The chemokine superfamily includes at least 20 receptors and more than 50 ligands [1-5]. The chemokine ligands can be separated into two major categories depending on whether they express a CC or CXC amino acid motif in their N-termini. This dichotomy appears to be functionally important since many CC chemokines preferentially target monocytes and T cells, while CXC chemokines such as IL-8 (CXCL8) tend to attract neutrophils. The CC chemokines bind to a family of G-protein coupled
Semiquantitative analysis of intrahepatic CC-chemokine mRNAs in chronic hepatitis C  [PDF]
Hans Dieter Nischalke,Jacob Nattermann,Hans-Peter Fischer,Tilman Sauerbruch,Ulrich Spengler,Franz Ludwig Dumoulin
Mediators of Inflammation , 2004, DOI: 10.1080/09629350400003159
Abstract: BACKGROUND: The mechanisms leading to hepatic injury in chronic hepatitis C virus (HCV) infection are only incompletely understood. Recent data propose a correlation of the intrahepatic expression of the CC chemokine RANTES and the degree of periportal and portal inflammatory liver damage.
CC Chemokine Receptor 5: The Interface of Host Immunity and Cancer  [PDF]
Carlos Eduardo Coral de Oliveira,Julie Massayo Maeda Oda,Roberta Losi Guembarovski,Karen Braj?o de Oliveira,Carolina Batista Ariza,Jamil Soni Neto,Bruna Karina Banin Hirata,Maria Angelica Ehara Watanabe
Disease Markers , 2014, DOI: 10.1155/2014/126954
Abstract: Solid tumors are embedded in a stromal microenvironment consisting of immune cells, such as macrophages and lymphocytes, as well as nonimmune cells, such as endothelial cells and fibroblasts. Chemokines are a type of small secreted chemotactic cytokine and together with their receptors play key roles in the immune defense. Critically, they regulate cancer cellular migration and also contribute to their proliferation and survival. The CCR5 chemokine receptor is involved in leucocytes chemotaxis to sites of inflammation and plays an important role in the macrophages, T cells, and monocytes recruitment. Additionally, CCR5 may have an indirect effect on cancer progression by controlling the antitumor immune response, since it has been demonstrated that its expression could promote tumor growth and contribute to tumor metastasis, in different types of malignant tumors. Furthermore, it was demonstrated that a CCR5 antagonist may inhibit tumor growth, consisting of a possible therapeutic target. In this context, the present review focuses on the establishment of CCR5 within the interface of host immunity, tumor microenvironment, and its potential as a targeting to immunotherapy. 1. Introduction Chemokines are a type of small secreted chemotactic cytokine. Together with their receptors, they play key roles in the immune defense by directing and controlling the migration, activation, differentiation, and survival in the physiology of acute and chronic inflammatory processes as well as in the pathological deregulations by attracting and simulating the various subsets of specific leukocytes [1]. Moreover, chemokines critically regulate cancer cellular migration and also contribute to their proliferation and survival [2]. The identification of a large number of chemokine receptors and their selectivity characterization and expression have provided information on the traffic regulation of leukocytes in health and disease. They are expressed on different types of leukocytes constitutively or induced, depending on cell types [3]. The chemokine system is often thought as showing significant redundancy since one receptor can bind multiple ligands, and conversely, a single ligand can bind several chemokine receptors [4]. However, differential spatio-temporal expression patterns for different chemokines and receptors in our body indicate that they probably have distinct roles in vivo [5]. To date, about 45 chemokines and 20 chemokine receptors have been identified and are grouped into four categories (C, CC, CXC, and CX3C) based on the location of the main cysteine
In vitro pharmacoregulation of CC chemokine ligand 5 and its receptor CCR5 in diffuse lung diseases  [PDF]
Veronika Sekerova,Daniela Subrtova,Frantisek Mrazek,Agata Gibejova,Vitezslav Kolek,Roland M. du Bois,Martin Petrek
Mediators of Inflammation , 2003, DOI: 10.1080/09629350310001599657
Abstract: Background: CC chemokine ligand (CCL)5 and its receptor CCR5 contribute to leukocyte migration into lungs of patients with diffuse lung diseases (DLD). Pharmacological regulation of CCL5 and CCR5 expression was therefore explored in bronchoalveolar cells obtained from patients with DLD.
CC-chemokine receptors: a potential therapeutic target for Trypanosoma cruzi-elicited myocarditis
Marino, APMP;Silva, AA;Santos, PVA;Pinto, LMO;Gazinelli, RT;Teixeira, MM;Lannes-Vieira, J;
Memórias do Instituto Oswaldo Cruz , 2005, DOI: 10.1590/S0074-02762005000900015
Abstract: the comprehension of the pathogenesis of trypanosoma cruzi-elicited myocarditis is crucial to delineate new therapeutic strategies aiming to ameliorate the inflammation that leads to heart dysfunction, without hampering parasite control. the augmented expression of ccl5/rantes and ccl3/mip-1a, and their receptor ccr5, in the heart of t. cruzi-infected mice suggests a role for cc-chemokines and their receptors in the pathogenesis of t. cruzi-elicited myocarditis. herein, we discuss our recent results using a cc-chemokine receptor inhibitor (met-rantes), showing the participation of cc-chemokines in t. cruzi infection and unraveling cc-chemokine receptors as an attractive therapeutic target for further evaluation in chagas disease.
Function of Chemokine (CXC Motif) Ligand 12 in Periodontal Ligament Fibroblasts  [PDF]
Yuichi Yashiro, Yoshiaki Nomura, Mikimoto Kanazashi, Koji Noda, Nobuhiro Hanada, Yoshiki Nakamura
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095676
Abstract: The periodontal ligament (PDL) is one of the connective tissues located between the tooth and bone. It is characterized by rapid turnover. Periodontal ligament fibroblasts (PDLFs) play major roles in the rapid turnover of the PDL. Microarray analysis of human PDLFs (HPDLFs) and human dermal fibroblasts (HDFs) demonstrated markedly high expression of chemokine (CXC motif) ligand 12 (CXCL12) in the HPDLFs. CXCL12 plays an important role in the migration of mesenchymal stem cells (MSCs). The function of CXCL12 in the periodontal ligament was investigated in HPDLFs. Expression of CXCL12 in HPDLFs and HDFs was examined by RT-PCR, qRT-PCR and ELISA. Chemotactic ability of CXCL12 was evaluated in both PDLFs and HDFs by migration assay of MSCs. CXCL12 was also immunohistochemically examined in the PDL in vivo. Expression of CXCL12 in the HPDLFs was much higher than that in HDFs in vitro. Migration assay demonstrated that the number of migrated MSCs by HPDLFs was significantly higher than that by HDFs. In addition, the migrated MSCs also expressed CXCL12 and several genes that are familiar to fibroblasts. CXCL12 was immunohistochemically localized in the fibroblasts in the PDL of rat molars. The results suggest that PDLFs synthesize and secrete CXCL12 protein and that CXCL12 induces migration of MSCs in the PDL in order to maintain rapid turnover of the PDL.
Role of CC chemokine CCL6/C10 as a monocyte chemoattractant in a murine acute peritonitis  [PDF]
Andrew M. LaFleur,Nicholas W. Lukacs,Steven L. Kunkel,Akihiro Matsukawa
Mediators of Inflammation , 2004, DOI: 10.1080/09629350400014172
Abstract: THE aim of this study was to determine the role of CC chemokine CCL6/C10 in acute inflammation. Intraperitoneal injection of thioglycollate increased peritoneal CCL6, which peaked at 4 h and remained elevated at 48 h. Neutralization of CCL6 significantly inhibited the macrophage infiltration (34-48% reduction), but not other cell types, without decreasing the other CC chemokines known to attract monocytes/macrophages. CCL6 was expressed in peripheral eosinophils and elicited macrophages, but not in elicited neutrophils. Peritoneal CCL6 level was not decreased in granulocyte-depleted mice where eosinophil influx was significantly impaired. Thus, CCL6 appears to contribute to the macrophage infiltration that is independent of other CC chemokines. Eosinophils pre-store CCL6, but do not release CCL6 in the peritoneum in this model of inflammation.
CC-Chemokine CCL15 Expression and Possible Implications for the Pathogenesis of IgE-Related Severe Asthma  [PDF]
Yasuo Shimizu,Kunio Dobashi
Mediators of Inflammation , 2012, DOI: 10.1155/2012/475253
Abstract: Airway inflammation is accompanied by infiltration of inflammatory cells and an abnormal response of airway smooth muscle. These cells secrete chemokines and express the cell surface chemokine receptors that play an important role in the migration and degranulation of inflammatory cells. Omalizumab is a monoclonal antibody directed against immunoglobulin E, and its blocking of IgE signaling not only reduces inflammatory cell infiltration mediated by the Th2 immune response but also inhibits other immune responses. The chemokine CCL15 is influenced by omalizumab, and the source of CCL15 has been reported to be airway smooth muscle cells and basophils. CCL15 binds to its receptor CCR1, which has been reported to be expressed by various inflammatory cells and also by airway smooth muscle cells. Therefore, CCL15/CCR1 signaling could be a target for the treatment of asthma. We review the role of CCL15 in the pathogenesis of asthma and also discuss the influence of IgE-mediated immunomodulation via CCL15 and its receptor CCR1. 1. Introduction Chemokines play an important role in the accumulation of inflammatory cells. They belong to a superfamily of small (6–14?kDa) proteins that regulate trafficking in various cells [1]. The C-C motif chemokine ligand 15 (CCL15) is a member of the macrophage inflammatory protein-1 family of chemokines, and its gene is located on 17q11.2. The genetic sequence of CCL15 is similar to that of C-C motif chemokine ligand 5 (CCL5) which is known as regulated on activation normal T cell expressed and secreted (RANTES) and C-C motif chemokine ligand 3 (CCL3), which is named macrophage inflammatory protein-1α (MIP-1α). The CCL15 gene has four exons and three introns. CCL15 has also been variously termed macrophage inhibitory protein-5 (MIP-5), leukotactin-1 (Lkn-1), and human C-C chemokine 2 (HCC-2) [2–4]. CCL15 binds to two receptors known as CCR1 and CCR3, but it has a higher affinity for the former [2, 5, 6]. Although other chemokines, such as CCL3L1 and CCL5, have already been examined in detail to assess their role in asthma, little is known about the possible influence of CCL15 on asthma. Recently, the serum level of CCL15 was found to be elevated in patients with severe asthma and it was shown to be reduced by omalizumab, a humanized anti-IgE antibody [7]. In addition, airway smooth muscle cells (ASMCs) have been shown to produce CCL15 in vitro, and these cells express CCR1 in asthma patients [8, 9]. This paper reviews the role of CCL15 in the pathogenesis of asthma and also discusses the influence of IgE-mediated
Chemokine (C-C motif) ligand 2 mediates direct and indirect fibrotic responses in human and murine cultured fibrocytes
Jason E Ekert, Lynne A Murray, Anuk M Das, Hai Sheng, Jill Giles-Komar, Michael A Rycyzyn
Fibrogenesis & Tissue Repair , 2011, DOI: 10.1186/1755-1536-4-23
Abstract: Following optimized and identical human and murine fibrocyte isolation, both cell sources were shown to be positive for CCR2 by flow cytometry and this expression colocalized with collagen I and CD45. Human blood fibrocytes stimulated with the CCR2 ligand chemokine (C-C motif) ligand 2 (CCL2), demonstrated increased proliferation (P < 0.005) and differentiation into myofibroblasts (P < 0.001), as well as a chemotactic response (P < 0.05). Murine fibrocytes also responded to CCR2 stimulation, with CCL12 being more potent than CCL2.This study directly compares the functional responses of human and murine fibrocytes to CCR2 ligands, and following comparable isolation techniques. We have shown comparable biological effects, strengthening the translatability of the murine models to human disease with respect to targeting the CCR2 axis to ameliorate disease in IPF patients.Fibrocytes are a population of circulating cells that have been reported to express a variety of markers including leukocyte markers (CD45, CD34), mesenchymal markers (collagen I, fibronectin) and chemokine receptors (chemokine (C-C motif) receptor 3 (CCR3), CCR5, CCR7 and C-X-C chemokine receptor type 4 (CXCR4)) [1]. Human and mouse studies have demonstrated that fibrocytes from peripheral blood migrate to skin wound chambers [1-3] and bronchial mucosa after antigen challenge [4]. Furthermore, these cells have been reported in disease states with fibrotic pathologies including hypertrophic scars, asthma and idiopathic pulmonary fibrosis (IPF) [4-7]. Fibrocytes are functionally pleiotropic, potentially contributing to fibrogenesis by directly producing collagen, as well as inflammatory cytokines, hematopoietic growth factors, and chemokines [6-10].In preclinical models of lung fibrosis, inhibition of various chemokine receptor/ligand pathways reduces lung fibrosis and it has been hypothesized to be in part due to a reduction in fibrocyte recruitment [6-9]. However, the effect of inhibiting specific chem
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