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248 results on '"Bingle, Lynne"'

10. LPLUNC1 Modulates Innate Immune Responses to Vibrio cholerae

Author

Shin, Ok S., Uddin, Taher, Citorik, Robert, Wang, Jennifer P., Pelle, Patricia Della, Kradin, Richard L., Bingle, Colin D., Bingle, Lynne, Camilli, Andrew, Bhuiyan, Taufiqur R., Shirin, Tahmina, Ryan, Edward T., Calderwood, Stephen B., Finberg, Robert W., Qadri, Firdausi, LaRocque, Regina C., and Harris, Jason B.

Published
2011
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26. Salivary BPIFA proteins are altered in patients undergoing hematopoietic cell transplantation.

Author

Innocentini, Lara Maria Alencar Ramos, Silva, Andreia Aparecida, Carvalho, Marco Antonio, Coletta, Ricardo D., Corrêa, Maria Elvira Pizzigatti, Bingle, Lynne, Bingle, Colin D., Vargas, Pablo Agustin, and Lopes, Márcio Ajudarte

Subjects
SALIVA analysis, PROTEINS, ANALYSIS of variance, IMMUNOHISTOCHEMISTRY, GENE expression, RESEARCH funding, HEMATOPOIETIC stem cell transplantation, DATA analysis software, LONGITUDINAL method
Abstract

Objective: The aim of this study was to evaluate the expression of BPIFA proteins in the saliva and salivary glands of hematopoietic cell transplant (HCT) patients. Material and Methods: This longitudinal study included patients who had undergone autologous HCT (auto‐HCT) and allogeneic HCT (allo‐HCT), and unstimulated saliva was collected at three time points, with a fourth collection at oral chronic graft‐versus‐host disease (cGVHD) onset. BPIFA expression was analysed by Western blotting in saliva and immunostaining in the minor salivary glands of cGVHD patients. Results: Auto‐HCT patients showed increased levels of BPIFA1 (p =.021) and BPIFA2 at D+7 (p =.040), whereas allo‐HCT group demonstrated decreased expression of BPIFA2 at D+8 (p =.002) and at D+80 (p =.001) and a significant association between BPIFA2 low levels and hyposalivation was observed (p =.02). BPIFA2 was significantly lower in the cGVHD patients when compared to baseline (p =.04). Conclusions: The results of this study show distinct pattern of expression of BPIF proteins in both auto‐HCT and allo‐HCT recipients with decreased levels of BPIFA2 during hyposalivation and cGVHD. Further studies are necessary to elucidate these proteins mechanisms and their clinical implications in these groups of patients. [ABSTRACT FROM AUTHOR]

Published
2022
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27. Directed Transport of CRP Across In Vitro Models of the Blood-Saliva Barrier Strengthens the Feasibility of Salivary CRP as Biomarker for Neonatal Sepsis

Author

Lin, Grace C., primary, Küng, Erik, additional, Smajlhodzic, Merima, additional, Domazet, Sandra, additional, Friedl, Heinz P., additional, Angerer, Joachim, additional, Wisgrill, Lukas, additional, Berger, Angelika, additional, Bingle, Lynne, additional, Peham, Johannes R., additional, and Neuhaus, Winfried, additional

Published
2021
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29. An In Vitro Barrier Model of the Human Submandibular Salivary Gland Epithelium Based on a Single Cell Clone of Cell Line HTB-41

Author

Lin, Grace C., Smajlhodzic, Merima, Bandian, Anna-Maria, Friedl, Heinz-Peter, Leitgeb, Tamara, Oerter, Sabrina, Stadler, Kerstin, Giese, Ulrich, Peham, Johannes R., Bingle, Lynne, Neuhaus, Winfried, and Publica

Subjects
rheumatoid arthritis, Submandibular, blood-saliva barrier, salivary gland, Sjögren's syndrome, periodontitis
Abstract

The blood-saliva barrier (BSB) consists of the sum of the epithelial cell layers of the oral mucosa and salivary glands. In vitro models of the BSB are inevitable to investigate and understand the transport of salivary biomarkers from blood to saliva. Up to now, standardized, cell line-based models of the epithelium of the submandibular salivary gland are still missing for this purpose. Therefore, we established epithelial barrier models of the submandibular gland derived from human cell line HTB-41 (A-253). Single clone isolation resulted in five different clones (B2, B4, B9, D3, and F11). Clones were compared to the parental cell line HTB-41 using measurements of the transepithelial electrical resistance (TEER), paracellular marker permeability assays and analysis of marker expression for acinar, ductal, and myoepithelial cells. Two clones (B9, D3) were characterized to be of acinar origin, one clone (F11) to be of myoepithelial origin and one isolation (B4) derived from two cells, to be presumably a mixture of acinar and ductal origin. Clone B2, presumably of ductal origin, showed a significantly higher paracellular barrier compared to other clones and parental HTB-41. The distinct molecular identity of clone B2 was confirmed by immunofluorescent staining, qPCR, and flow cytometry. Experiments with ferritin, a biomarker for iron storage, demonstrated the applicability of the selected model based on clone B2 for transport studies. In conclusion, five different clones originating from the submandibular gland cell line HTB-41 were successfully characterized and established as epithelial barrier models. Studies with the model based on the tightest clone B2 confirmed its suitability for transport studies in biomarker research.

Published
2020

30. TrkB-targeted therapy for mucoepidermoid carcinoma

Author

Wagner, Vivian Petersen, Martins, Manoela Domingues, Amoura, Esra, Zanella, Virgilio Gonzales, Roesler, Rafael, De-Farias, Caroline Brunetto, Bingle, Colin D., Vargas, Pablo Agustin, and Bingle, Lynne

Subjects
Salivary gland neoplasms, Terapêutica, Cell biology, Neoplasias de cabeça e pescoço, Receptor trkB, Biologia celular, Neoplasias das glandulas salivares, Therapeutics, Adenocarcinoma, Carcinoma Mucoepidermoide, Head and neck neoplasms
Abstract

The brain-derived neurotrophic factor (BDNF)/tyrosine receptor kinase B (TrkB) pathway was previously associated with key oncogenic outcomes in a number of adenocarcinomas. The aim of our study was to determine the role of this pathway in mucoepidermoid carcinoma (MEC). Three MEC cell lines (UM-HMC-2, H253 and H292) were exposed to Cisplatin, the TrkB inhibitor, ANA-12 and a combination of these drugs. Ultrastructural changes were assessed through transmission electron microscopy; scratch and Transwell assays were used to assess migration and invasion; and a clonogenic assay and spheroid-forming assay allowed assessment of survival and percentage of cancer stem cells (CSC). Changes in cell ultrastructure demonstrated Cisplatin cytotoxicity, while the effects of ANA-12 were less pronounced. Both drugs, used individually and in combination, delayed MEC cell migration, invasion and survival. ANA-12 significantly reduced the number of CSC, but the Cisplatin effect was greater, almost eliminating this cell population in all MEC cell lines. Interestingly, the spheroid forming capacity recovered, following the combination therapy, as compared to Cisplatin alone. Our studies allowed us to conclude that the TrkB inhibition, efficiently impaired MEC cell migration, invasion and survival in vitro, however, the decrease in CSC number, following the combined treatment of ANA-12 and Cisplatin, was less than that seen with Cisplatin alone; this represents a limiting factor.

Published
2020

31. TrkB-Targeted Therapy for Mucoepidermoid Carcinoma

Author

Wagner, Vivian P., primary, Martins, Manoela D., additional, Amoura, Esra, additional, Zanella, Virgilio G., additional, Roesler, Rafael, additional, de Farias, Caroline B., additional, Bingle, Colin D., additional, Vargas, Pablo A., additional, and Bingle, Lynne, additional

Published
2020
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42. An In Vitro Barrier Model of the Human Submandibular Salivary Gland Epithelium Based on a Single Cell Clone of Cell Line HTB-41: Establishment and Application for Biomarker Transport Studies

Author

Lin, Grace C., primary, Smajlhodzic, Merima, additional, Bandian, Anna-Maria, additional, Friedl, Heinz-Peter, additional, Leitgeb, Tamara, additional, Oerter, Sabrina, additional, Stadler, Kerstin, additional, Giese, Ulrich, additional, Peham, Johannes R., additional, Bingle, Lynne, additional, and Neuhaus, Winfried, additional

Published
2020
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50. Differential epithelial expression of the putative innate immune molecule SPLUNC1 in Cystic Fibrosis

Author

Wallace William A, Rassl Doris, Cross Simon S, Barnes Frances A, Bingle Lynne, Campos Michael A, and Bingle Colin D

Subjects
Diseases of the respiratory system, RC705-779
Abstract

Abstract Introduction Short PLUNC1 (SPLUNC1) is the founding member of a family of proteins (PLUNCS) expressed in the upper respiratory tract and oral cavity, which may function in host defence. It is one of the most highly expressed genes in the upper airways and the protein has been detected in sputum and nasal secretions. The biology of the PLUNC family is poorly understood but in keeping with the putative function of the protein as an immune defence protein, a number of RNA and protein studies have indicated that SPLUNC1 is increased in inflammatory/infectious conditions such as Cystic Fibrosis (CF), COPD and allergic rhinitis. Methods We used immunohistochemistry to localise SPLUNC1 in lung tissue from patients with CF and a range of other lung diseases. We used a range of additional markers for distinct cell types to try to establish the exact site of secretion of SPLUNC1. We have complemented these studies with a molecular analysis of SPLUNC1 gene expression in primary human lung cell cultures and isolated inflammatory cell populations. Results In CF, expression of SPLUNC1 is significantly elevated in diseased airways and positive staining was noted in some of the inflammatory infiltrates. The epithelium of small airways of CF lung exhibit significantly increased SPLUNC1 staining compared to similar sized airways in non-CF lungs where staining is absent. Strong staining was also seen in mucous plugs in the airways, these included many inflammatory cells. No alveolar epithelial staining was noted in CF tissue. Airway epithelial staining did not co-localise with MUC5AC suggesting that the protein was not produced by goblet cells. Using serial sections stained with neutrophil elastase and CD68 we could not demonstrate co-localisation of SPLUNC1 with either neutrophils or macrophages/monocytes, indicating that these cells were not a source of SPLUNC1 in the airways of CF lungs. No change in staining pattern was noted in the small airways or lung parenchyma of other lung diseases studied including, COPD, emphysema or pneumonia where significant NE and CD68 staining was noted. Cultures of primary tracheobronchial epithelial cells were analysed by RT-PCR and showed that pro-inflammatory mediators did not induce expression of SPLUNC1. We have also shown that SPLUNC1 gene expression was not seen in isolated human mononuclear cells, macrophages or neutrophils. Conclusion These studies show that SPLUNC1 is specifically and significantly increased in the small airways of lungs from patients with CF. They further suggest that it is the airway epithelium that is responsible for the increased levels of SPLUNC1 in CF and not inflammatory cells; this could be a defensive response to the infectious component of the disease.

Published
2007
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