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14 results on '"Looi K"'

1. MAPPING AND IDENTIFYING MIGRATION PATTERN DIFFERENCES IN RESPONSE TO WOUNDING IN ASTHMATIC AND NON-ASTHMATIC AIRWAY EPITHELIAL CELLS

Author

Iosifidis, T., Buckley, A., Sutanto, E., Ling, K., Looi, K., Garratt, L., Kicic-Starcevich, E., Martinovich, K., Shaw, N., Montgomery, S., Vijayasekaran, S., Lannigan, F., Rigby, P., Knight, D., Stick, S., Kicic, Anthony, Iosifidis, T., Buckley, A., Sutanto, E., Ling, K., Looi, K., Garratt, L., Kicic-Starcevich, E., Martinovich, K., Shaw, N., Montgomery, S., Vijayasekaran, S., Lannigan, F., Rigby, P., Knight, D., Stick, S., and Kicic, Anthony

Published
2016

2. DETERMINING THE FUNDAMENTALS IN EPITHELIAL BARRIER INTEGRITY AND FUNCTION IN PAEDIATRIC ASTHMA

Author

Looi, K., Buckley, A., Rigby, P., Garratt, L., Iosifidis, T., Lannigan, F., Knight, D., Zosky, G., Larcombe, A., Ling, K., Martinovich, K., Kicic-Starcevich, E., Shaw, N., Sutanto, E., Kicic, Anthony, Stick, S., Looi, K., Buckley, A., Rigby, P., Garratt, L., Iosifidis, T., Lannigan, F., Knight, D., Zosky, G., Larcombe, A., Ling, K., Martinovich, K., Kicic-Starcevich, E., Shaw, N., Sutanto, E., Kicic, Anthony, and Stick, S.

Published
2016

3. Dysregulated innate immune response pathways in children with cystic fibrosis following human rhinovirus infection

Author

Ling, K., Seferali, A., Gill, E., Garratt, L., Sutanto, E., Montgomery, S., Starcevich-Kicic, E., Lannigan, F., Looi, K., Iosifidis, T., Martinovich, K., Shaw, N., Hancock, R., Turvey, S., Kicic, Anthony, Stick, S., Ling, K., Seferali, A., Gill, E., Garratt, L., Sutanto, E., Montgomery, S., Starcevich-Kicic, E., Lannigan, F., Looi, K., Iosifidis, T., Martinovich, K., Shaw, N., Hancock, R., Turvey, S., Kicic, Anthony, and Stick, S.

Published
2016

4. DISASSEMBLY OF EPITHELIAL TIGHT JUNCTIONS IN WELL-DIFFERENTIATED AIR-LIQUID INTERFACE (ALI) CULTURES FOLLOWING HUMAN RHINOVIRUS INFECTION RESULTS IN AIRWAY EPITHELIAL PERMEABILITY CHANGES

Author

Looi, K., Buckley, A., Rigby, P., Garratt, L., Iosifidis, T., Lannigan, F., Knight, D., Zosky, G., Larcombe, A., Ling, K., Martinovich, K., Kicic-Starcevich, E., Shaw, N., Sutanto, E., Stick, S., Kicic, Anthony, Looi, K., Buckley, A., Rigby, P., Garratt, L., Iosifidis, T., Lannigan, F., Knight, D., Zosky, G., Larcombe, A., Ling, K., Martinovich, K., Kicic-Starcevich, E., Shaw, N., Sutanto, E., Stick, S., and Kicic, Anthony

Published
2015

5. EFFECTS OF HUMAN RHINOVIRUS INFECTION IN LARGE AND SMALL AIRWAY OF LUNG TRANSPLANT RECIPIENTS

Author

Ling, K., Lavendar, M., Musk, M., Wrobel, J., Garratt, L., Martinovich, K., Shaw, N., Iosifidis, T., Looi, K., Kicic-Starcevich, E., Lannigan, F., Hopkins, P., Chambers, D., Sutanto, E., Stick, S., Kicic, Anthony, Ling, K., Lavendar, M., Musk, M., Wrobel, J., Garratt, L., Martinovich, K., Shaw, N., Iosifidis, T., Looi, K., Kicic-Starcevich, E., Lannigan, F., Hopkins, P., Chambers, D., Sutanto, E., Stick, S., and Kicic, Anthony

Published
2015

6. INVESTIGATION OF MIGRATION MARKERS IN LEADING EDGE CELLS DURING AIRWAY WOUND REPAIR

Author

Iosifidis, T., Buckley, A., Sutanto, E., Ling, K., Garratt, L., Looi, K., Kicic-Starcevich, E., Martinovich, K., Dye, D., Coombe, Deirdre, Lannigan, F., Rigby, P., Knight, D., Stick, S., Kicic, Anthony, Iosifidis, T., Buckley, A., Sutanto, E., Ling, K., Garratt, L., Looi, K., Kicic-Starcevich, E., Martinovich, K., Dye, D., Coombe, Deirdre, Lannigan, F., Rigby, P., Knight, D., Stick, S., and Kicic, Anthony

Published
2015

7. Conditionally reprogrammed primary airway epithelial cells successfully maintain lineage, phenotypic and functional characteristics

Author

Martinovich, K., Iosifidis, T., Ling, K., Sutanto, E., Kicic-Starcevich, E., Looi, K., Garrat, L., Shaw, N., Buckley, A., Lannigan, F., Knight, D., Stick, S., Kicic, Anthony, Martinovich, K., Iosifidis, T., Ling, K., Sutanto, E., Kicic-Starcevich, E., Looi, K., Garrat, L., Shaw, N., Buckley, A., Lannigan, F., Knight, D., Stick, S., and Kicic, Anthony

Published
2015

8. Effects of human rhinovirus on epithelial barrier integrity and function in children with asthma.

Author

Looi, K., Buckley, A. G., Rigby, P. J., Garratt, L. W., Iosifidis, T., Zosky, G. R., Larcombe, A. N., Lannigan, F. J., Ling, K.‐m., Martinovich, K. M., Kicic‐starcevich, E., Shaw, N. C., Sutanto, E. N., Knight, D. A., Kicic, A., and Stick, S. M.

Subjects
*COMMON cold, *ASTHMA in children, *BRONCHIAL diseases, *TIGHT junctions, *IMMUNOCYTOCHEMISTRY, *PATIENTS
Abstract

Summary: Background: Bronchial epithelial tight junctions (TJ) have been extensively assessed in healthy airway epithelium. However, no studies have yet assessed the effect of human rhinovirus (HRV) infection on the expression and resultant barrier function in epithelial tight junctions (TJ) in childhood asthma. Objectives: To investigate the impact of HRV infection on airway epithelial TJ expression and barrier function in airway epithelial cells (AECs) of children with and without asthma. Furthermore, to test the hypothesis that barrier integrity and function is compromised to a greater extent by HRV in AECs from asthmatic children. Methods: Primary AECs were obtained from children with and without asthma, differentiated into air ‐liquid interface (ALI) cultures and infected with rhinovirus. Expression of claudin‐1, occludin and zonula occluden‐1 (ZO‐1) was assessed via qPCR, immunocytochemistry (ICC), in‐cell western (ICW) and confocal microscopy. Barrier function was assessed by transepithelial electrical resistance (TER; RT) and permeability to fluorescent dextran. Results: Basal TJ gene expression of claudin‐1 and occludin was significantly upregulated in asthmatic children compared to non‐asthmatics; however, no difference was seen with ZO‐1. Interestingly, claudin‐1, occludin and ZO‐1 protein expression was significantly reduced in AEC of asthmatic children compared to non‐asthmatic controls suggesting possible post‐transcriptional inherent differences. HRV infection resulted in a transient dissociation of TJ and airway barrier integrity in non‐asthmatic children. Although similar dissociation of TJ was observed in asthmatic children, a significant and sustained reduction in TJ expression concurrent with both a significant decrease in TER and an increase in permeability in asthmatic children was observed. Conclusion: This study demonstrates novel intrinsic differences in TJ gene and protein expression between AEC of children with and without asthma. Furthermore, it correlates directly the relationship between HRV infection and the resultant dissociation of epithelial TJ that causes a continued altered barrier function in children with asthma. [ABSTRACT FROM AUTHOR]

Published
2018
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10. DYSREGULATED REPAIR AND EPITHELIAL INJURY IN SMALL AND LARGE AIRWAYS OF LUNG TRANSPLANT PATIENTS IS AMELIORATED BY AZITHROMYCIN

Author

Kicic, Anthony, Lavender, M., Musk, M., Wrobel, J., Banerjee, B., Ling, K., Martinovich, K., Garratt, L., Iosifidis, T., Looi, K., Kicic-Starvevich, E., Lannigan, F., Hopkins, P., Yerkovich, S., Sutanto, E., Chambers, D., Stick, S., Kicic, Anthony, Lavender, M., Musk, M., Wrobel, J., Banerjee, B., Ling, K., Martinovich, K., Garratt, L., Iosifidis, T., Looi, K., Kicic-Starvevich, E., Lannigan, F., Hopkins, P., Yerkovich, S., Sutanto, E., Chambers, D., and Stick, S.

Published
2014

13. INFLUENZA INFECTION FACILITATES ALLERGIC SENSITIZATION

Author

Perks, K., Looi, K., Stick, S.M., Kicic, Anthony, Iosifidis, T., Berry, L.J., Zosky, G.R., Larcombe, Alexander, Perks, K., Looi, K., Stick, S.M., Kicic, Anthony, Iosifidis, T., Berry, L.J., Zosky, G.R., and Larcombe, Alexander

Published
2013

14. Impaired airway epithelial cell responses from children with asthma to rhinoviral infection.

Author

Kicic, A., Stevens, P. T., Sutanto, E. N., Kicic‐Starcevich, E., Ling, K.‐M., Looi, K., Martinovich, K. M., Garratt, L. W., Iosifidis, T., Shaw, N. C., Buckley, A. G., Rigby, P. J., Lannigan, F. J., Knight, D. A., and Stick, S. M.

Subjects
EPITHELIAL cells, RHINOVIRUSES, AIRWAY (Anatomy), ASTHMATICS, CYTOKINES, INTERFERONS
Abstract

Background The airway epithelium forms an effective immune and physical barrier that is essential for protecting the lung from potentially harmful inhaled stimuli including viruses. Human rhinovirus ( HRV) infection is a known trigger of asthma exacerbations, although the mechanism by which this occurs is not fully understood. Objective To explore the relationship between apoptotic, innate immune and inflammatory responses to HRV infection in airway epithelial cells ( AECs) obtained from children with asthma and non-asthmatic controls. In addition, to test the hypothesis that aberrant repair of epithelium from asthmatics is further dysregulated by HRV infection. Methods Airway epithelial brushings were obtained from 39 asthmatic and 36 non-asthmatic children. Primary cultures were established and exposed to HRV1b and HRV14. Virus receptor number, virus replication and progeny release were determined. Epithelial cell apoptosis, IFN-β production, inflammatory cytokine release and epithelial wound repair and proliferation were also measured. Results Virus proliferation and release was greater in airway epithelial cells from asthmatics but this was not related to the number of virus receptors. In epithelial cells from asthmatic children, virus infection dampened apoptosis, reduced IFN-β production and increased inflammatory cytokine production. HRV1b infection also inhibited wound repair capacity of epithelial cells isolated from non-asthmatic children and exaggerated the defective repair response seen in epithelial cells from asthmatics. Addition of IFN-β restored apoptosis, suppressed virus replication and improved repair of airway epithelial cells from asthmatics but did not reduce inflammatory cytokine production. Conclusions Collectively, HRV infection delays repair and inhibits apoptotic processes in epithelial cells from non-asthmatic and asthmatic children. The delayed repair is further exaggerated in cells from asthmatic children and is only partially reversed by exogenous IFN-β. [ABSTRACT FROM AUTHOR]

Published
2016
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