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1. An innovative in silico model of the oral mucosa reveals the impact of extracellular spaces on chemical permeation through epithelium

Author

Edwards, Sean M., Harding, Amy L., Leedale, Joseph A., Webb, Steve D., Colley, Helen E., Murdoch, Craig, and Bearon, Rachel N.

Subjects
Quantitative Biology - Tissues and Organs
Abstract

In pharmaceutical therapeutic design or toxicology, accurately predicting the permeation of chemicals through human epithelial tissues is crucial, where permeation is significantly influenced by the tissue's cellular architecture. Current mathematical models for multi-layered epithelium such as the oral mucosa only use simplistic 'bricks and mortar' geometries and therefore do not account for the complex cellular architecture of these tissues at the microscale level, such as the extensive plasma membrane convolutions that define the extracellular spaces between cells. Chemicals often permeate tissues via this paracellular route, meaning that permeation is underestimated. To address this, measurements of human buccal mucosal tissue were conducted to ascertain the width and tortuosity of extracellular spaces across the epithelium. Using mechanistic mathematical modelling, we show that the convoluted geometry of extracellular spaces significantly impacts chemical permeation and that this can be approximated, provided that extracellular tortuosity is accounted for. We next developed an advanced physically-relevant in silico model of oral mucosal chemical permeation using partial differential equations, fitted to chemical permeation in vitro assays on tissue-engineered human oral mucosa. Tissue geometries were measured and captured in silico, and permeation examined and predicted for chemicals with different physicochemical properties. The effect of altering the extracellular space to mimic permeation enhancers was also assessed by perturbing the in silico model. This novel in vitro-in silico approach has the potential to expedite pharmaceutical innovation for testing oromucosal chemical permeation, providing a more accurate, physiologically-relevant model which can reduce animal testing with early screening based on chemical properties.

Published
2024

6. Candidalysin Is Required for Neutrophil Recruitment and Virulence During Systemic Candida albicans Infection

Author

Swidergall, Marc, Khalaji, Mina, Solis, Norma V, Moyes, David L, Drummond, Rebecca A, Hube, Bernhard, Lionakis, Michail S, Murdoch, Craig, Filler, Scott G, and Naglik, Julian R

Subjects
Infectious Diseases, Aetiology, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Inflammatory and immune system, Infection, Good Health and Well Being, Animals, Candida albicans, Candidiasis, Invasive, Cytokines, Disease Models, Animal, Endothelial Cells, Female, Fungal Proteins, Male, Mice, Inbred BALB C, Neutrophil Infiltration, Signal Transduction, Survival Analysis, Virulence, Virulence Factors, Zebrafish, candidalysin, fungal, systemic, endothelial, Candida albicans, Biological Sciences, Medical and Health Sciences, Microbiology
Abstract

BackgroundCandidalysin is a cytolytic peptide toxin secreted by Candida albicans hyphae and has significantly advanced our understanding of fungal pathogenesis. Candidalysin is critical for mucosal C albicans infections and is known to activate epithelial cells to induce downstream innate immune responses that are associated with protection or immunopathology during oral or vaginal infections. Furthermore, candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes. However, the role of candidalysin in driving systemic infections is unknown.MethodsIn this study, using candidalysin-producing and candidalysin-deficient C albicans strains, we show that candidalysin activates mitogen-activated protein kinase (MAPK) signaling and chemokine secretion in endothelial cells in vitro.ResultsCandidalysin induces immune activation and neutrophil recruitment in vivo, and it promotes mortality in zebrafish and murine models of systemic fungal infection.ConclusionsThe data demonstrate a key role for candidalysin in neutrophil recruitment and fungal virulence during disseminated systemic C albicans infections.

Published
2019

20. Supplementary Figure 2 from Use of Macrophages to Target Therapeutic Adenovirus to Human Prostate Tumors

Author

Muthana, Munitta, primary, Giannoudis, Athina, primary, Scott, Simon D., primary, Fang, Hsin-Yu, primary, Coffelt, Seth B., primary, Morrow, Fiona J., primary, Murdoch, Craig, primary, Burton, Julian, primary, Cross, Neil, primary, Burke, Bernard, primary, Mistry, Roshna, primary, Hamdy, Freddie, primary, Brown, Nicola J., primary, Georgopoulos, Lindsay, primary, Hoskin, Peter, primary, Essand, Magnus, primary, Lewis, Claire E., primary, and Maitland, Norman J., primary

Published
2023
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22. Supplementary Figure 4 from Use of Macrophages to Target Therapeutic Adenovirus to Human Prostate Tumors

Author

Muthana, Munitta, primary, Giannoudis, Athina, primary, Scott, Simon D., primary, Fang, Hsin-Yu, primary, Coffelt, Seth B., primary, Morrow, Fiona J., primary, Murdoch, Craig, primary, Burton, Julian, primary, Cross, Neil, primary, Burke, Bernard, primary, Mistry, Roshna, primary, Hamdy, Freddie, primary, Brown, Nicola J., primary, Georgopoulos, Lindsay, primary, Hoskin, Peter, primary, Essand, Magnus, primary, Lewis, Claire E., primary, and Maitland, Norman J., primary

Published
2023
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23. Supplementary Figure Legends 1-5, Methods from Angiopoietin-2 Regulates Gene Expression in TIE2-Expressing Monocytes and Augments Their Inherent Proangiogenic Functions

Author

Coffelt, Seth B., primary, Tal, Andrea O., primary, Scholz, Alexander, primary, De Palma, Michele, primary, Patel, Sunil, primary, Urbich, Carmen, primary, Biswas, Subhra K., primary, Murdoch, Craig, primary, Plate, Karl H., primary, Reiss, Yvonne, primary, and Lewis, Claire E., primary

Published
2023
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25. Supplementary Figure 1 from Use of Macrophages to Target Therapeutic Adenovirus to Human Prostate Tumors

Author

Muthana, Munitta, primary, Giannoudis, Athina, primary, Scott, Simon D., primary, Fang, Hsin-Yu, primary, Coffelt, Seth B., primary, Morrow, Fiona J., primary, Murdoch, Craig, primary, Burton, Julian, primary, Cross, Neil, primary, Burke, Bernard, primary, Mistry, Roshna, primary, Hamdy, Freddie, primary, Brown, Nicola J., primary, Georgopoulos, Lindsay, primary, Hoskin, Peter, primary, Essand, Magnus, primary, Lewis, Claire E., primary, and Maitland, Norman J., primary

Published
2023
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27. Supplementary Figure 3 from Use of Macrophages to Target Therapeutic Adenovirus to Human Prostate Tumors

Author

Muthana, Munitta, primary, Giannoudis, Athina, primary, Scott, Simon D., primary, Fang, Hsin-Yu, primary, Coffelt, Seth B., primary, Morrow, Fiona J., primary, Murdoch, Craig, primary, Burton, Julian, primary, Cross, Neil, primary, Burke, Bernard, primary, Mistry, Roshna, primary, Hamdy, Freddie, primary, Brown, Nicola J., primary, Georgopoulos, Lindsay, primary, Hoskin, Peter, primary, Essand, Magnus, primary, Lewis, Claire E., primary, and Maitland, Norman J., primary

Published
2023
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28. Supplementary Figure 5 from Use of Macrophages to Target Therapeutic Adenovirus to Human Prostate Tumors

Author

Muthana, Munitta, primary, Giannoudis, Athina, primary, Scott, Simon D., primary, Fang, Hsin-Yu, primary, Coffelt, Seth B., primary, Morrow, Fiona J., primary, Murdoch, Craig, primary, Burton, Julian, primary, Cross, Neil, primary, Burke, Bernard, primary, Mistry, Roshna, primary, Hamdy, Freddie, primary, Brown, Nicola J., primary, Georgopoulos, Lindsay, primary, Hoskin, Peter, primary, Essand, Magnus, primary, Lewis, Claire E., primary, and Maitland, Norman J., primary

Published
2023
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29. Data from Use of Macrophages to Target Therapeutic Adenovirus to Human Prostate Tumors

Author

Muthana, Munitta, primary, Giannoudis, Athina, primary, Scott, Simon D., primary, Fang, Hsin-Yu, primary, Coffelt, Seth B., primary, Morrow, Fiona J., primary, Murdoch, Craig, primary, Burton, Julian, primary, Cross, Neil, primary, Burke, Bernard, primary, Mistry, Roshna, primary, Hamdy, Freddie, primary, Brown, Nicola J., primary, Georgopoulos, Lindsay, primary, Hoskin, Peter, primary, Essand, Magnus, primary, Lewis, Claire E., primary, and Maitland, Norman J., primary

Published
2023
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30. ‘Cytology-on-a-chip’ based sensors for monitoring of potentially malignant oral lesions

Author

Abram, Timothy J., Floriano, Pierre N., Christodoulides, Nicolaos, James, Robert, Kerr, A. Ross, Thornhill, Martin H., Redding, Spencer W., Vigneswaran, Nadarajah, Speight, Paul M., Vick, Julie, Murdoch, Craig, Freeman, Christine, Hegarty, Anne M., D’Apice, Katy, Phelan, Joan A., Corby, Patricia M., Khouly, Ismael, Bouquot, Jerry, Demian, Nagi M., Weinstock, Y. Etan, Rowan, Stephanie, Yeh, Chih-Ko, McGuff, H. Stan, Miller, Frank R., Gaur, Surabhi, Karthikeyan, Kailash, Taylor, Leander, Le, Cathy, Nguyen, Michael, Talavera, Humberto, Raja, Rameez, Wong, Jorge, and McDevitt, John T.

Published
2016
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31. Interobserver agreement in dysplasia grading: toward an enhanced gold standard for clinical pathology trials

Author

Speight, Paul M., Abram, Timothy J., Floriano, Pierre N., James, Robert, Vick, Julie, Thornhill, Martin H., Murdoch, Craig, Freeman, Christine, Hegarty, Anne M., D'Apice, Katy, Kerr, A. Ross, Phelan, Joan, Corby, Patricia, Khouly, Ismael, Vigneswaran, Nadarajah, Bouquot, Jerry, Demian, Nagi M., Weinstock, Y. Etan, Redding, Spencer W., Rowan, Stephanie, Yeh, Chih-Ko, McGuff, H. Stan, Miller, Frank R., and McDevitt, John T.

Published
2015
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37. List of contributors

Author

Akbari, Zahra, primary, Almeida, Luis, additional, Almela, Thafar, additional, Amdjadi, Parisa, additional, Amrollahi, Pouya, additional, Ansari, Sahar, additional, Bader, Rizwan, additional, Baghaban Eslaminejad, Mohamadreza, additional, Bardsley, Katie, additional, Bencharit, Sompop, additional, Bindal, Priyadarshni, additional, Boccaccini, Aldo R., additional, Borkent, Dewi, additional, Brook, Ian, additional, Chai, Wen L., additional, Colley, Helen, additional, Crawford, Aileen, additional, Dabbagh, Ali, additional, Dashtimoghadarm, Erfan, additional, Dehghani, Shima, additional, Del Monico, Michael, additional, Dentino, Andrew R., additional, El-Bialy, Tarek, additional, El-Wassefy, Noha A., additional, Fahimipour, Farahnaz, additional, Fahmy, Mina D., additional, Faldu, Jasmine, additional, Farahani, Masomeh, additional, Farahat, Dina S., additional, Fatehinya, Atena, additional, Golzar, Hossein, additional, Gonzalez, Jose, additional, Goudouri, Ourania-Menti, additional, Hearnden, Vanessa, additional, Hopkinson, Louise, additional, Hosseini, Samaneh, additional, Ibrahim, Mohamed S., additional, Ivanovski, Saso, additional, Jafari, Maissa, additional, Jahangir, Shahrbanoo, additional, Jazayeri, Hossein E., additional, Abu Kasim, Noor H., additional, Khojasteh, Arash, additional, Khoshroo, Kimia, additional, Khurshid, Zohaib, additional, Kontonasaki, Eleana, additional, Lam, Lisetta, additional, Lee, Ryan S.B., additional, Mazafari, Masoud, additional, Moghadam, Farzaneh, additional, Moharamzadeh, Keyvan, additional, Moshaverinia, Alireza, additional, Murdoch, Craig, additional, Najeeb, Shariq, additional, Nazeman, Pantea, additional, Nejatian, Touraj, additional, Nicholson, Zach, additional, Omidi, Maysam, additional, Omidi, Meisam, additional, Paknejad, Zahrasadat, additional, Ramasamy, Thamil Selvee, additional, Rasoulianboroujeni, Morteza, additional, Rezai Rad, Maryam, additional, Salehi-Nik, Nasim, additional, Sefat, Farshid, additional, Seifi, Massoud, additional, Shah, Brinda, additional, Shahmoradi, Saleheh, additional, Tahriri, Mohammadreza, additional, Tayebi, Lobat, additional, Vashaee, Daryoosh, additional, Wirth, Jonathan, additional, Wu, Benjamin M., additional, Yadegari, Amir, additional, Yao, Wiley, additional, Yazdian, Fatemeh, additional, Yazdimamaghani, Mostafa, additional, S. Zafar, Muhammad, additional, Zahedi, Ehsan, additional, and Zohaib, Sana, additional

Published
2017
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39. Immune mechanisms in oral lichen planus.

Author

El‐Howati, Asma, Thornhill, Martin H., Colley, Helen E., and Murdoch, Craig

Subjects
ORAL lichen planus, CELLULAR signal transduction, IMMUNITY
Abstract

Oral lichen planus (OLP) is a T cell‐mediated inflammatory disease of the oral mucosa that has been extensively researched over many years but as yet the mechanisms of pathogenesis are still not fully understood. Whilst the specific aetiological factors driving OLP remain ambiguous, evidence points to the development of a chronic, dysregulated immune response to OLP‐mediating antigens presented by innate immune cells and oral keratinocytes leading to increased cytokine, chemokine and adhesion molecule expression. These molecules recruit T cells and mast cells to the diseased site and orchestrate a complex interplay between cells that culminates in keratinocyte cell death, mucosal basement membrane destruction and long‐term chronicity of the disease. The main lymphocytes involved are thought to be CD8+ cytotoxic and CD4+ Th1 polarised T cells although recent evidence indicates the involvement of other Th subsets such as Th9, Th17 and Tregs, suggesting that a more complex immune cell relationship exists during the disease process. This review provides an overview of the immune mechanisms at play in OLP pathogenesis with particular emphasis on the role of the different Th subsets and how these recent discoveries may guide research towards identifying potential therapeutic targets. [ABSTRACT FROM AUTHOR]

Published
2023
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41. c‐Src activation as a potential marker of chemical‐induced skin irritation using tissue‐engineered skin equivalents.

Author

Harding, Amy L., Colley, Helen E., Vazquez, Inmaculada Barragan, Danby, Simon, Hasan, Md Zobaer, Nakanishi, Hirofumi, Furuno, Tetsuo, and Murdoch, Craig

Subjects
CELLULAR signal transduction, LACTIC acid, CHEMICAL potential, KINASES, BETAINE, ACTIVATION (Chemistry)
Abstract

Skin irritancy to topically applied chemicals is a significant problem that affects millions of people worldwide. New or modified chemical entities must be tested for potential skin irritancy by industry as part of the safety and toxicity profiling process. Many of these tests have now moved to a non‐animal‐based format to reduce experiments on animals. However, these tests for irritancy potential often rely on monolayer cultures of keratinocytes that are not representative of the skin architecture or tissue‐engineered human skin equivalents (HSE) using complex multi‐gene expression panels that are often cumbersome and not amenable for high throughput. Here, we show that human skin equivalents increase abundance of several phosphorylated kinases (c‐Src, c‐Jun, p53, GSK3α/β) in response to irritant chemical stimulation by phosphokinase array analysis. Specific phosphorylation of c‐SrcY419 was confirmed by immunoblotting and was plasma membrane‐associated in basal/spinous cells by phospho‐specific immunohistochemistry. Moreover, c‐SrcY419 phosphorylation in response to the irritants lactic acid and capsaicin was inhibited by the c‐Src inhibitors KB‐SRC and betaine trimethylglycine. These data provide the first evidence for c‐Src specific activation in response to chemical irritants and point to the development of new modes of rapid testing by immunodetection for first‐pass screening of potential irritants. This study demonstrates that specific kinases, in particular c‐Src, are activated in HSE in response to chemical irritants. The rapid increase in specific phosphorylated signal transduction molecules upon exposure to irritants may prove ideal targets to rapidly identify and differentiate potential chemical irritants from non‐irritants. [ABSTRACT FROM AUTHOR]

Published
2023
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50. The IL‐1/IL‐1R axis induces greater fibroblast‐derived chemokine release in human papillomavirus‐negative compared to positive oropharyngeal cancer

Author

Al‐Sahaf, Sarmad, Hunter, Keith D., Bolt, Robert, Ottewell, Penelope D., and Murdoch, Craig

Subjects
Receptors, Interleukin-1 Type I, Papillomavirus Infections, virus diseases, Tumor Immunology and Microenvironment, Fibroblasts, female genital diseases and pregnancy complications, fibroblast, stomatognathic diseases, Chemotaxis, Leukocyte, Oropharyngeal Neoplasms, Cell Line, Tumor, cytokine, Tumor Microenvironment, Humans, head and neck cancer, Chemokines, human papillomavirus, tumour microenvironment, leukocyte, Interleukin-1
Abstract

Human papillomavirus (HPV) is now recognised as a major aetiological agent in the pathogenesis of oropharyngeal carcinoma (OPC). HPV‐positive tumours are associated with better outcomes compared to HPV‐negative tumours, possibly due to differences in their aetiology and/or the tumour microenvironment. Increased numbers of tumour‐associated leukocytes have been observed in many cancers including OPC, with variable influence on prognosis depending on the leukocyte subpopulation investigated. Whether HPV status influences leukocyte recruitment to OPC remains unknown. This in‐vitro study examined differences in the chemoattractant capacity of HPV‐positive and HPV‐negative OPC cell lines. Gene and protein expression analysis demonstrated that whilst both monocultures of HPV‐positive and HPV‐negative cell lines, along with normal tonsillar fibroblasts (NTF), expressed low chemokine levels, NTF cultured with conditioned medium from HPV‐negative OPC cells expressed significantly higher levels of all chemokines tested compared to NTF incubated with the medium from HPV‐positive OPC cell lines. HPV‐negative OPC lines expressed IL‐1β mRNA whereas HPV‐positive cells did not, and NTF constitutively expressed IL‐1R1. Pre‐treatment with the IL‐R antagonist, anakinra or siRNA to IL‐1R1 significantly reduced chemokine secretion from NTF stimulated with conditioned medium from HPV‐negative tumour cells or recombinant IL‐1β (p < 0.05). These data suggest that secretion of chemokines is driven by the interaction between HPV‐negative OPC cells and stromal fibroblasts through an IL‐1/IL‐1R‐mediated mechanism that is less prominent within the HPV‐positive tumour microenvironment. These observations may explain differences in leukocyte sub‐populations recruited to HPV‐positive versus negative OPC and indicate that HPV status is a key determinant in controlling the inflammatory tumour microenvironment., What's new? Rates of oropharyngeal cancer (OPC) are increasing, mainly due to human papillomavirus (HPV) infection. There is limited understanding, however, about the affects of HPV status in OPC on tumor‐stromal interactions, which influence tumor development and progression. In this study, HPV‐negative OPC cells were found to drive a robust chemokine secretion profile in stromal tonsillar fibroblasts, whereas HPV‐positive OPC cells exhibited relatively low chemokine expression. Increased chemokine expression in stromal tonsillar fibroblasts was mediated by the IL‐1/IL‐1R axis. The findings suggest that HPV status plays a role in the recruitment of leukocyte sub‐populations in the OPC tumor microenvironment, influencing inflammatory activity.

Published
2018

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