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257 results on '"Bingle, Colin D."'

53. Association of innate defense proteins BPIFA1 and BPIFB1 with disease severity in COPD

Author

De Smet,Elise G, Seys,Leen JM, Verhamme,Fien M, Vanaudenaerde,Bart M, Brusselle,Guy G, Bingle,Colin D, Bracke,Ken R, De Smet,Elise G, Seys,Leen JM, Verhamme,Fien M, Vanaudenaerde,Bart M, Brusselle,Guy G, Bingle,Colin D, and Bracke,Ken R

Abstract

Elise G De Smet,1 Leen JM Seys,1,2 Fien M Verhamme,1 Bart M Vanaudenaerde,3 Guy G Brusselle,1 Colin D Bingle,4 Ken R Bracke1 1Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium; ²Laboratory of Immunoregulation and Mucosal Immunology, VIB-UGent Center for Inflammation Research, Ghent, Belgium; 3Laboratory for Respiratory Diseases, Department of Clinical and Experimental Medicine, KU Leuven, Leuven, Belgium; 4Academic Unit of Respiratory Medicine, Department of Infection, Immunity and Cardiovascular Disease, The University of Sheffield, Sheffield, UK Abstract: Chronic obstructive pulmonary disease (COPD) is characterized by an abnormal inflammatory response in the lungs caused by the inhalation of noxious particles and gases. The airway epithelium has a protective function against these harmful agents by maintaining a physical barrier and by secreting defensive proteins, such as bactericidal/permeability-increasing fold-containing (BPIF) proteins, BPIFA1 and BPIFB1. However, inconsistent data regarding BPIFA1 expression in smokers and COPD patients have been reported to date. Therefore, we investigated the expression of BPIFA1 and BPIFB1 in a large cohort of never-smokers and smokers with and without COPD, both on the messenger RNA (mRNA) level in lung tissue and on the protein level in airway epithelium. Furthermore, we examined the correlation between BPIFA1 and BPIFB1 levels, goblet cell hyperplasia, and lung function measurements. BPIFA1 and BPIFB1 mRNA expressions were significantly increased in stage III–IV COPD patients compared with stage II COPD patients and subjects without COPD. In addition, protein levels in COPD patients were significantly increased in comparison with subjects without COPD. BPIFA1 and BPIFB1 levels were inversely correlated with measurements of airflow limitation and positively correlated with goblet cell hyperplasia. In

Published
2017

54. Absence or mislocalization of DNAH5 is a characteristic marker for motile ciliary abnormality in nasal polyps

Author

Qiu, Qianhui, primary, Peng, Yang, additional, Zhu, Zhenchao, additional, Chen, Zhuo, additional, Zhang, Chi, additional, Ong, Hsiao Hui, additional, Tan, Kai Sen, additional, Hong, Haiyu, additional, Yan, Yan, additional, Huang, Haoqi, additional, Liu, Jing, additional, Li, Xianqing, additional, Nam, H. N., additional, Dung, N. T. N., additional, Shi, Li, additional, Yang, Qintai, additional, Bingle, Colin D., additional, and Wang, De-Yun, additional

Published
2017
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56. Mcidas mutant mice reveal a two-step process for the specification and differentiation of multiciliated cells in mammals.

Author

Hao Lu, Anujan, Priyanka, Feng Zhou, Yiliu Zhang, Yan Ling Chong, Bingle, Colin D., and Roy, Sudipto

Subjects
CILIA & ciliary motion, CELL differentiation, MAMMALS
Abstract

Motile cilia on multiciliated cells (MCCs) function in fluid clearance over epithelia. Studies with Xenopus embryos and individuals with the congenital respiratory disorder reduced generation of multiple motile cilia (RGMC), have implicated the nuclear protein MCIDAS (MCI), in the transcriptional regulation of MCC specification and differentiation. Recently, a paralogous protein, geminin coiled-coil domain containing (GMNC), was also shown to be required for MCC formation. Surprisingly, in contrast to the presently held view, we find that Mci mutant mice can specify MCC precursors. However, these precursors cannot produce multiple basal bodies, and mature into single ciliated cells. We identify an essential role for MCI in inducing deuterosome pathway components for the production of multiple basal bodies. Moreover, GMNC and MCI associate differentially with the cell-cycle regulators E2F4 and E2F5, which enables them to activate distinct sets of target genes (ciliary transcription factor genes versus basal body amplification genes). Our data establish a previously unrecognized two-step model for MCC development: GMNC functions in the initial step for MCC precursor specification. GMNC induces Mci expression that drives the second step of basal body production for multiciliation. [ABSTRACT FROM AUTHOR]

Published
2019
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58. An in vitro model of murine middle ear epithelium

Author

Mulay, Apoorva, primary, Akram, Khondoker, additional, Williams, Debbie, additional, Armes, Hannah, additional, Russell, Catherine, additional, Hood, Derek, additional, Armstrong, Stuart, additional, Stewart, James P., additional, Brown, Steve D. M., additional, Bingle, Lynne, additional, and Bingle, Colin D., additional

Published
2016
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59. Absence or mislocalization of DNAH5 is a characteristic marker for motile ciliary abnormality in nasal polyps.

Author

Qiu, Qianhui, Peng, Yang, Zhu, Zhenchao, Chen, Zhuo, Zhang, Chi, Ong, Hsiao Hui, Tan, Kai Sen, Hong, Haiyu, Yan, Yan, Huang, Haoqi, Liu, Jing, Li, Xianqing, Nam, H. N., Dung, N. T. N., Shi, Li, Yang, Qintai, Bingle, Colin D., Wang, De‐Yun, and Wang, De-Yun

Abstract

Objective: Motile cilia impairment is a common condition in patients with chronically inflamed airways, such as is seen in nasal polyps (NPs). The mechanism underlying this pathogenic condition is complex and not fully understood.Methods: We investigated the presence and localization of dynein axonemal heavy chain 5 (DNAH5) in motile cilia using immunofluorescence staining in paraffin-embedded nasal biopsies from NPs (n = 120) and inferior turbinate mucosa (n = 35) of healthy controls. We also performed single-cell staining on cytospin samples (NP = 5, control = 5). Three patterns of DNAH5 localization are defined, including pattern A (presence throughout the axoneme), pattern B (undetectable in the distal part of the axoneme), and pattern C (completely missing throughout the entire axoneme). We developed a semiquantitative scoring system for which 0 = (pattern A > 70%); 1 = (patterns A + B > 70%); and 2 = (pattern C ≥ 30%) in each high-power field (5 fields per sample).Results: Based on our DNAH5 scoring system, the median (1st and 3rd quartile) score was 0.3 (0.2 and 0.4) for samples from controls, and 1.1 (0.6 and 1.6) for samples from NPs in paraffin specimens (P < 0.001). The DNAH5 score had a significant positive relationship with the Lund-Mackay computed tomography score (r = 0.329, P = 0.005) and was higher in patients with eosinophilic NPs (P = 0.006). For cytospin samples, the mean percentage of patterns A, B, and C were 74%, 14%, and 12% in controls, and 48%, 20%, and 32% in NPs, respectively.Conclusion: Our results suggest that the absence or mislocalization of DNAH5 from motile cilia is a common and potentially important pathological phenomenon in chronically inflamed airway epithelium.Level Of Evidence: NA. Laryngoscope, 128:E97-E104, 2018. [ABSTRACT FROM AUTHOR]

Published
2018
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61. Inhibition of neutrophil apoptosis by ATP is mediated by the P2Y11 receptor1

Author

Vaughan, Kathryn R., Stokes, Leanne, Prince, Lynne R., Meis, Sabine, Kassack, Matthias U., Bingle, Colin D., Sabroe, Ian, Surprenant, Annmarie, and Whyte, Moira K.B.

Subjects
Adenosine Triphosphate, Neutrophils, Receptors, Purinergic P2, Purinergic P2 Receptor Antagonists, Humans, Apoptosis, Calcium, Calcium Signaling, Suramin, Cyclic AMP-Dependent Protein Kinases, Article, Cells, Cultured
Abstract

Neutrophils undergo rapid constitutive apoptosis that is delayed by a range of pathogen- and host-derived inflammatory mediators. We have investigated the ability of the nucleotide ATP, to which neutrophils are exposed both in the circulation and at sites of inflammation, to modulate the lifespan of human neutrophils. We found that physiologically relevant concentrations of ATP cause a concentration-dependent delay of neutrophil apoptosis (assessed by morphology, annexin V/To-Pro3 staining, and mitochondrial membrane permeabilization). We found that even brief exposure to ATP (10 min) was sufficient to cause a long-lasting delay of apoptosis and showed that the effects were not mediated by ATP breakdown to adenosine. The P2 receptor mediating the antiapoptotic actions of ATP was identified using a combination of more selective ATP analogs, receptor expression studies, and study of downstream signaling pathways. Neutrophils were shown to express the P2Y11 receptor and inhibition of P2Y11 signaling using the antagonist NF157 abrogated the ATP-mediated delay of neutrophil apoptosis, as did inhibition of type I cAMP-dependent protein kinases activated downstream of P2Y11, without effects on constitutive apoptosis. Specific targeting of P2Y11 could retain key immune functions of neutrophils but reduce the injurious effects of increased neutrophil longevity during inflammation.

Published
2007

82. Acceleration of Human Neutrophil Apoptosis by TRAIL

Author

Renshaw, Stephen A., primary, Parmar, Jasvir S., additional, Singleton, Vanessa, additional, Rowe, Sarah J., additional, Dockrell, David H., additional, Dower, Steven K., additional, Bingle, Colin D., additional, Chilvers, Edwin R., additional, and Whyte, Moira K. B., additional

Published
2003
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99. Phylogenetic and evolutionary analysis of the PLUNC gene family.

Author

Bingle, Colin D., LeClair, Elizabeth E., Havard, Suzanne, Bingle, Lynne, Gillingham, Paul, and Craven, C. Jeremy

Abstract

The PLUNC family of human proteins are candidate host defense proteins expressed in the upper airways. The family subdivides into short (SPLUNC) and long (LPLUNC) proteins, which contain domains predicted to be structurally similar to one or both of the domains of bactericidal/permeability-increasing protein (BPI), respectively. In this article we use analysis of the human, mouse, and rat genomes and other sequence data to examine the relationships between the PLUNC family proteins from humans and other species, and between these proteins and members of the BPI family. We show that PLUNC family clusters exist in the mouse and rat, with the most significant diversification in the locus occurring for the short PLUNC family proteins. Clear orthologous relationships are established for the majority of the proteins, and ambiguities are identified. Completion of the prediction of the LPLUNC4 proteins reveals that these proteins contain approximately a 150-residue insertion encoded by an additional exon. This insertion, which is predicted to be largely unstructured, replaces the structure homologous to the 40s hairpin of BPI. We show that the exon encoding this region is anomalously variable in size across the LPLUNC proteins, suggesting that this region is key to functional specificity. We further show that the mouse and human PLUNC family orthologs are evolving rapidly, which supports the hypothesis that these proteins are involved in host defense. Intriguingly, this rapid evolution between the human and mouse sequences is replaced by intense purifying selection in a large portion of the N-terminal domain of LPLUNC4. Our data provide a basis for future functional studies of this novel protein family. [ABSTRACT FROM AUTHOR]

Published
2004
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