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2. Matrix metalloproteinase-7 is increased in lung bases but not apices in idiopathic pulmonary fibrosis

Author

Jaffar, Jade, Wong, Mae, Fishbein, Gregory A, Alhamdoosh, Monther, McMillan, Laura, Gamell-Fulla, Cristina, Ng, Milica, Wilson, Nick, Symons, Karen, Glaspole, Ian, and Westall, Glen

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Lung, Autoimmune Disease, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Cardiovascular medicine and haematology, Oncology and carcinogenesis
Abstract

IntroductionIdiopathic pulmonary fibrosis (IPF) is a progressively fibrotic lung condition with poor prognosis. Matrix metalloproteinase-7 (MMP7) is a protein secreted by epithelial cells in IPF lungs. It is not known if MMP7 expression correlates with fibrotic changes in lung tissue.MethodsTissue samples from lung apices and bases were obtained from 20 IPF patients and 14 non-diseased control (NDC) donors. In formalin-fixed paraffin-embedded sections, histological assessment of fibrosis was performed; overall MMP7 positivity was assessed by immunohistochemistry and MMP7+ cells were quantified using multiplex immunohistochemistry. Protein expression of MMP7 in whole lung lysates was quantified by Western blotting. Bulk tissue transcriptomic profiles of 101 samples were analysed using RNA sequencing technologies.ResultsLung tissue from IPF bases was more fibrotic than in apices. MMP7 protein is elevated in IPF lung base tissue. In IPF whole lung lysates, MMP7 protein levels are increased compared to NDC donors and was increased in IPF lung bases compared to apices. MMP7 protein levels correlated with MMP7 gene expression levels in lung tissue. MMP7 transcript levels were increased in IPF base compared to NDC base lung tissue and increased in IPF base tissue compared to IPF apex tissue.ConclusionsOur cross-sectional study suggests that lung epithelial MMP7 expression increases as the tissue becomes more fibrotic and identifies a potentially nonepithelial or immune-cell source. Mechanisms of disease progression in IPF are still unclear, and our study suggests aberrant MMP7 production may be a histological starting point of lung tissue fibrosis.

Published
2022

8. Defining a natural killer cell-enriched molecular rejection-like state in lung transplant transbronchial biopsies

Author

Gauthier, Patrick T., Mackova, Martina, Hirji, Alim, Weinkauf, Justin, Timofte, Irina L., Snell, Greg I., Westall, Glen P., Havlin, Jan, Lischke, Robert, Zajacová, Andrea, Simonek, Jan, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, Halloran, Kieran, and Halloran, Philip F.

Published
2023
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10. A Systematically Derived Exposure Assessment Instrument for Chronic Hypersensitivity Pneumonitis

Author

Barnes, Hayley, Morisset, Julie, Molyneaux, Philip, Westall, Glen, Glaspole, Ian, Collard, Harold R, Collaborators, CHP Exposure Assessment, Antoniou, Katerina M, Barber, Christopher M, Behr, Jürgen, Bonella, Francesco, Corte, Tamera, Costabel, Ulrich, Cottin, Vincent, Crestani, Bruno, Dalphin, Jean-Charles, Flaherty, Kevin R, Goh, Nicole, Johannson, Kerri A, Kondoh, Yasuhiro, Lederer, David, Lee, Joyce, Maher, Toby M, Martinez, Fernando J, Morell, Ferran, Noth, Imre, Raghu, Ganesh, Renzoni, Elisabetta, Richeldi, Luca, Ryerson, Christopher J, Ryu, Jay H, Salisbury, Margaret L, Singh, Sheetu, Selman, Moises, Strek, Mary E, Tarlo, Susan M, Tomassetti, Sara, Vancheri, Carlo, Vasakova, Martina, Wolters, Paul, and Wells, Athol

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Management of diseases and conditions, 7.3 Management and decision making, Alveolitis, Extrinsic Allergic, Chronic Disease, Consensus, Humans, Lung, Tomography, X-Ray Computed, extrinsic allergic alveolitis, hypersensitivity pneumonitis, interstitial lung diseases, CHP Exposure Assessment Collaborators, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundChronic hypersensitivity pneumonitis (CHP) is an immune-mediated interstitial lung disease (ILD) caused by inhalational exposure to environmental antigens, resulting in parenchymal fibrosis. By definition, a diagnosis of CHP assumes a history of antigen exposure, but only half of all patients eventually diagnosed with CHP will have a causative antigen identified. Individual clinician variation in eliciting a history of antigen exposure may affect the frequency and confidence of CHP diagnosis.MethodsA list of potential causative exposures were derived from a systematic review of the literature. A Delphi method was applied to an international panel of ILD experts to obtain consensus regarding technique for the elicitation of exposure to antigens relevant to a diagnosis of CHP. The consensus threshold was set at 80% agreement, and median ≤ 2, interquartile range = 0 on a 5-point Likert scale (1, strongly agree; 2, tend to agree; 3, neither agree nor disagree; 4, disagree; 5, strongly disagree).ResultsIn two rounds, 36/40 experts participated. Experts agreed on 18 exposure items to ask every patient with suspected CHP. Themes included CHP inducing exposures, features that contribute to an exposure's relevance, and quantification of a relevant exposure. Based on the results from the literature review and Delphi process, a CHP exposure assessment instrument was derived. Using cognitive interviews, the instrument was revised by patients with ILD for readability and usability.ConclusionsThis Delphi survey provides items that ILD experts agree are important to ask in all patients presenting with suspected CHP and provides basis for a systematically derived CHP exposure assessment instrument. Clinical utility of this exposure assessment instrument may be affected by different local prevalence patterns of exposures. Ongoing research is required to clinically validate these items and consider their impact in more geographically diverse settings.

Published
2020

11. The molecular features of chronic lung allograft dysfunction in lung transplant airway mucosa

Author

Halloran, Kieran, Mackova, Martina, Parkes, Michael D, Hirji, Alim, Weinkauf, Justin, Timofte, Irina L, Snell, Greg I, Westall, Glen P, Lischke, Robert, Zajacova, Andrea, Havlin, Jan, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, and Halloran, Philip F

Published
2022
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16. Transcripts associated with chronic lung allograft dysfunction in transbronchial biopsies of lung transplants

Author

Parkes, Michael D., Halloran, Kieran, Hirji, Alim, Pon, Shane, Weinkauf, Justin, Timofte, Irina L., Snell, Greg I., Westall, Glen P., Havlin, Jan, Lischke, Robert, Zajacová, Andrea, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, and Halloran, Philip F.

Published
2022
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17. Emerging concepts of CMV in transplantation.

Author

Westall, Glen P., Gottlieb, David, Hughes, Peter, Marinelli, Tina, Rawlinson, William D., Ritchie, David, Sasadeusz, Joe, and Yong, Michelle K.

Subjects
*STEM cell transplantation, *CYTOMEGALOVIRUS diseases, *TRANSPLANTATION of organs, tissues, etc., *IMMUNOCOMPROMISED patients, *CELLULAR therapy
Abstract

Cytomegalovirus (CMV) infections continue to be associated with significant morbidity and mortality following solid organ transplantation and haemopoietic stem cell transplantation. Advances in understanding the biology of CMV in the immunosuppressed host will translate into improved management approaches and better clinical outcomes. Updated definitions of resistant and refractory CMV infections will lead to more consistent reporting of CMV outcomes, better inform appropriate antiviral strategies and influence clinical trial design. Improved knowledge of the immunological control of CMV in the immunosuppressed host has led to novel diagnostics, emerging therapeutic cellular therapies and the development of an informed rationale for prophylactic and pre‐emptive strategies. As the boundaries of transplantation are extended, new patterns of CMV infection are being recognised. Finally, recent studies support the use of novel antiviral therapies in transplant recipients in the appropriate clinical setting. In this review, we provide an update on important new and emerging concepts in the management of CMV in immunosuppressed transplant recipients. [ABSTRACT FROM AUTHOR]

Published
2024
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22. CD8+ T cells specific for an immunodominant SARS-CoV-2 nucleocapsid epitope display high naive precursor frequency and TCR promiscuity

Author

Nguyen, Thi H.O., Rowntree, Louise C., Petersen, Jan, Chua, Brendon Y., Hensen, Luca, Kedzierski, Lukasz, van de Sandt, Carolien E., Chaurasia, Priyanka, Tan, Hyon-Xhi, Habel, Jennifer R., Zhang, Wuji, Allen, Lilith F., Earnest, Linda, Mak, Kai Yan, Juno, Jennifer A., Wragg, Kathleen, Mordant, Francesca L., Amanat, Fatima, Krammer, Florian, Mifsud, Nicole A., Doolan, Denise L., Flanagan, Katie L., Sonda, Sabrina, Kaur, Jasveen, Wakim, Linda M., Westall, Glen P., James, Fiona, Mouhtouris, Effie, Gordon, Claire L., Holmes, Natasha E., Smibert, Olivia C., Trubiano, Jason A., Cheng, Allen C., Harcourt, Peter, Clifton, Patrick, Crawford, Jeremy Chase, Thomas, Paul G., Wheatley, Adam K., Kent, Stephen J., Rossjohn, Jamie, Torresi, Joseph, and Kedzierska, Katherine

Published
2021
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25. Molecular T-cell‒mediated rejection in transbronchial and mucosal lung transplant biopsies is associated with future risk of graft loss

Author

Halloran, Kieran, Parkes, Michael D., Timofte, Irina, Snell, Gregory, Westall, Glen, Havlin, Jan, Lischke, Robert, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, Hirji, Alim, Weinkauf, Justin, and Halloran, Philip F.

Published
2020
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28. A Systematically Derived Exposure Assessment Instrument for Chronic Hypersensitivity Pneumonitis

Author

Antoniou, Katerina M., Barber, Christopher M., Behr, Jürgen, Bonella, Francesco, Corte, Tamera, Costabel, Ulrich, Cottin, Vincent, Crestani, Bruno, Dalphin, Jean-Charles, Flaherty, Kevin R., Goh, Nicole, Johannson, Kerri A., Kondoh, Yasuhiro, Lederer, David, Lee, Joyce, Maher, Toby M., Martinez, Fernando J., Morell, Ferran, Noth, Imre, Raghu, Ganesh, Renzoni, Elisabetta, Richeldi, Luca, Ryerson, Christopher J., Ryu, Jay H., Salisbury, Margaret L., Singh, Sheetu, Selman, Moises, Strek, Mary E., Tarlo, Susan M., Tomassetti, Sara, Vancheri, Carlo, Vasakova, Martina, Wolters, Paul, Wells, Athol, Barnes, Hayley, Morisset, Julie, Molyneaux, Philip, Westall, Glen, Glaspole, Ian, and Collard, Harold R.

Published
2020
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35. Clinical outcomes of lung transplant recipients with telomerase mutations.

Author

Tokman, Sofya, Singer, Jonathan P, Devine, Megan S, Westall, Glen P, Aubert, John-David, Tamm, Michael, Snell, Gregory I, Lee, Joyce S, Goldberg, Hilary J, Kukreja, Jasleen, Golden, Jeffrey A, Leard, Lorriana E, Garcia, Christine K, and Hays, Steven R

Subjects
Humans, Pulmonary Fibrosis, Telomerase, Treatment Outcome, Lung Transplantation, Retrospective Studies, Graft Rejection, Mutation, Middle Aged, Female, Male, lung transplantation, pulmonary fibrosis, telomerase mutations, telomere, telomere syndrome, Transplantation, Rare Diseases, Kidney Disease, Clinical Research, Digestive Diseases, Genetics, Lung, Organ Transplantation, Liver Disease, Evaluation of treatments and therapeutic interventions, 6.4 Surgery, Renal and urogenital, Respiratory, Cardiorespiratory Medicine and Haematology, Surgery
Abstract

BackgroundSuccessful lung transplantation for patients with pulmonary fibrosis from telomerase mutations may be limited by systemic complications of telomerase dysfunction, including myelosuppression, cirrhosis, and malignancy. We describe clinical outcomes in 14 lung transplant recipients with telomerase mutations.MethodsSubjects underwent lung transplantation between February 2005 and April 2014 at 5 transplant centers. Data were abstracted from medical records, focusing on outcomes reflecting post-transplant treatment effects likely to be complicated by telomerase mutations.ResultsThe median age of subjects was 60.5 years (interquartile range = 52.0-62.0), 64.3% were male, and the mean post-transplant observation time was 3.2 years (SD ± 2.9). A mutation in telomerase reverse transcriptase was present in 11 subjects, a telomerase RNA component mutation was present in 2 subjects, and an uncharacterized mutation was present in 1 subject. After lung transplantation, 10 subjects were leukopenic and 5 did not tolerate lymphocyte anti-proliferative agents. Six subjects developed recurrent lower respiratory tract infections, 7 developed acute cellular rejection (A1), and 4 developed chronic lung allograft dysfunction. Eight subjects developed at least 1 episode of acute renal failure and 10 developed chronic renal insufficiency. In addition, 3 subjects developed cancer. No subjects had cirrhosis. At data censorship, 13 subjects were alive.ConclusionsThe clinical course for lung transplant recipients with telomerase mutations is complicated by renal disease, leukopenia with intolerance of lymphocyte anti-proliferative agents, and recurrent lower respiratory tract infections. In contrast, cirrhosis was absent, acute cellular rejection was mild, and development of chronic lung allograft dysfunction was comparable to other lung transplant recipients. Although it poses challenges, lung transplantation may be feasible for patients with pulmonary fibrosis from telomerase mutations.

Published
2015

36. CD8+ T cell landscape in Indigenous and non-Indigenous people restricted by influenza mortality-associated HLA-A*24:02 allomorph

Author

Hensen, Luca, Illing, Patricia T., Bridie Clemens, E., Nguyen, Thi H. O., Koutsakos, Marios, van de Sandt, Carolien E., Mifsud, Nicole A., Nguyen, Andrea T., Szeto, Christopher, Chua, Brendon Y., Halim, Hanim, Rizzetto, Simone, Luciani, Fabio, Loh, Liyen, Grant, Emma J., Saunders, Phillipa M., Brooks, Andrew G., Rockman, Steve, Kotsimbos, Tom C., Cheng, Allen C., Richards, Michael, Westall, Glen P., Wakim, Linda M., Loudovaris, Thomas, Mannering, Stuart I., Elliott, Michael, Tangye, Stuart G., Jackson, David C., Flanagan, Katie L., Rossjohn, Jamie, Gras, Stephanie, Davies, Jane, Miller, Adrian, Tong, Steven Y. C., Purcell, Anthony W., and Kedzierska, Katherine

Published
2021
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39. HLA‐C mismatching improves outcomes following lung transplantation.

Author

Hiho, Steven J., Levvey, Bronwyn J., Diviney, Mary B., Brooks, Andrew G., Holdsworth, Rhonda, Snell, Gregory I., Westall, Glen P., and Sullivan, Lucy C.

Subjects
LUNG transplantation, HISTOCOMPATIBILITY class I antigens, KILLER cell receptors, KILLER cells, LINKAGE disequilibrium
Abstract

HLA (HLA) are a major barrier to transplant success, as HLA‐A and ‐B molecules are principal ligands for T‐cells, and HLA‐C for Killer cell Immunoglobulin‐like Receptors (KIR), directing Natural Killer (NK) cell function. HLA‐C molecules are designated "C1" or "C2" ligands based on residues 77 and 80, which determine the NK cell responses. Here, we investigated donor/recipient HLA‐C mismatch associations with the development of chronic lung allograft dysfunction (CLAD) following lung transplantation (LTx). 310 LTx donor/recipient pairs were Next Generation Sequenced and assessed for C1 and C2 allotypes. PIRCHE scores were used to quantify HLA mismatching between donor/recipients at amino acid level and stratify recipients into low, moderate or highly mismatched groups (n = 103–104). Associations between C ligands and freedom from CLAD was assessed with Cox regression models and survival curves. C2/C2 recipients (n = 42) had less CLAD than those with C1/C1 (n = 138) or C1/C2 genotypes (n = 130) (p < 0.05). Incidence of CLAD was lower in C2/C2 recipients receiving a mismatched C1/C1 allograft (n = 14), compared to matched (n = 8) or heterozygous (n = 20) allografts. Furthermore, ~80% of these recipients (C2/C2 recipients receiving C1/C1 transplants) remained CLAD‐free for 10 years post‐LTx. Recipients with higher HLA‐C mismatching had less CLAD (p < 0.05) an observation not explained by linkage disequilibrium with other HLA loci. Our data implicates a role for HLA‐C in CLAD development. HLA‐C mismatching was not detrimental to LTx outcome, but potentially beneficial, representing a paradigm shift in assessing donor/recipient matching. This may inform better selection of donor/recipient pairs and potentially more targeted approaches to treating CLAD. [ABSTRACT FROM AUTHOR]

Published
2024
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40. SHIFTing goals in cystic fibrosis—managing extrapulmonary disease in the era of CFTR modulator therapy; Proceedings of the International Shaping Initiatives and Future Trends (SHIFT) Symposium.

Author

O'Donnell, Jonathan E. M., Hastings, Lucy A., Briody, Julie N., Chan, Christine L., Colombo, Carla, Douglas, Tonia A., Freedman, Steven D., Gonska, Tanja, Greenfield, Jerry R., Leung, Daniel H., Lim, Adeline Y. L., Moran, Antoinette, Prentice, Bernadette J., Putman, Melissa S., Trotter, Michael, Tullis, Elizabeth, Westall, Glen P., Verge, Charles F., Wainwright, Claire E., and Ooi, Chee Y.

Published
2024
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41. Platelet Activating Factor Receptor and Intercellular Adhesion Molecule–1 Expression Increases in the Small Airway Epithelium and Parenchyma of Patients with Idiopathic Pulmonary Fibrosis: Implications for Microbial Pathogenesis.

Author

Shahzad, Affan Mahmood, Lu, Wenying, Dey, Surajit, Bhattarai, Prem, Gaikwad, Archana Vijay, Jaffar, Jade, Westall, Glen, Sutherland, Darren, Singhera, Gurpreet Kaur, Hackett, Tillie-Louise, Eapen, Mathew Suji, and Sohal, Sukhwinder Singh

Subjects
PLATELET activating factor, CELL adhesion, ALVEOLAR macrophages, EPITHELIUM, METHACHOLINE chloride, IMMUNOSTAINING, IDIOPATHIC pulmonary fibrosis
Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is an irreversible lung fibrotic disorder of unknown cause. It has been reported that bacterial and viral co-infections exacerbate disease pathogenesis. These pathogens use adhesion molecules such as platelet activating factor receptor (PAFR) and intercellular adhesion molecule-1 (ICAM–1) to gain cellular entry, causing infections. Methods: Immunohistochemical staining was carried out for lung resections from IPF patients (n = 11) and normal controls (n = 12). The quantification of PAFR and ICAM–1 expression is presented as a percentage in the small airway epithelium. Also, type 2 pneumocytes and alveolar macrophages were counted as cells per mm2 of the parenchymal area and presented as a percentage. All image analysis was done using Image Pro Plus 7.0 software. Results: PAFR expression significantly increased in the small airway epithelium (p < 0.0001), type 2 pneumocytes (p < 0.0001) and alveolar macrophages (p < 0.0001) compared to normal controls. Similar trend was observed for ICAM–1 expression in the small airway epithelium (p < 0.0001), type 2 pneumocytes (p < 0.0001) and alveolar macrophages (p < 0.0001) compared to normal controls. Furthermore, the proportion of positively expressed type 2 pneumocytes and alveolar macrophages was higher in IPF than in normal control. Conclusions: This is the first study to show PAFR and ICAM–1 expression in small airway epithelium, type 2 pneumocytes and alveolar macrophages in IPF. These findings could help intervene microbial impact and facilitate management of disease pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Chronic Lung Allograft Dysfunction is Associated with an Increased Number of Non-HLA Antibodies

Author

Xu, Qingyong, primary, Elrefaei, Mohamed, additional, Taupin, Jean-Luc, additional, Hitchman, Kelley MK, additional, Hiho, Steven, additional, Gareau, Alison, additional, Iasella, Carlo, additional, Marrari, Marilyn, additional, Belousova, Natalia, additional, Bettinotti, Maria, additional, Narula, Tathagat, additional, Alvarez, Francisco, additional, Sanchez, Pablo G., additional, Levvey, Bronwyn, additional, Westall, Glen, additional, Snell, Gregory, additional, Levine, Deborah J., additional, Zeevi, Adriana, additional, and Roux, Antoine, additional

Published
2023
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46. The Utility of the Stanford Integrative Psychosocial Assessment for Transplant (SIPAT) in Predicting Outcomes Before and After Lung Transplantation

Author

Westall, Glen P, primary, Barnes, Hayley, additional, Levin, Kovi, additional, Gaffney, Nicole, additional, Harris, Jane, additional, Martinez, Otto, additional, Emsley, Christie, additional, Fuller, Louise, additional, Levvey, Bronwyn, additional, Snell, Greg I, additional, and Winton-Brown, Toby, additional

Published
2023
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49. Human CD8+ T cell cross-reactivity across influenza A, B and C viruses

Author

Koutsakos, Marios, Illing, Patricia T., Nguyen, Thi H. O., Mifsud, Nicole A., Crawford, Jeremy Chase, Rizzetto, Simone, Eltahla, Auda A., Clemens, E. Bridie, Sant, Sneha, Chua, Brendon Y., Wong, Chinn Yi, Allen, E. Kaitlynn, Teng, Don, Dash, Pradyot, Boyd, David F., Grzelak, Ludivine, Zeng, Weiguang, Hurt, Aeron C., Barr, Ian, Rockman, Steve, Jackson, David C., Kotsimbos, Tom C., Cheng, Allen C., Richards, Michael, Westall, Glen P., Loudovaris, Thomas, Mannering, Stuart I., Elliott, Michael, Tangye, Stuart G., Wakim, Linda M., Rossjohn, Jamie, Vijaykrishna, Dhanasekaran, Luciani, Fabio, Thomas, Paul G., Gras, Stephanie, Purcell, Anthony W., and Kedzierska, Katherine

Published
2019
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50. TGF-β1, pSmad-2/3, Smad-7, and β-catenin are augmented in IPF pulmonary arteries: potential role in driving endothelial to mesenchymal transition (EndMT)

Author

Lu, Wenying, primary, Gaikwad, Archana Vijay, additional, Chia, Collin, additional, Larby, Josie, additional, Haug, Greg, additional, Dey, Surajit, additional, Bhattarai, Prem, additional, Jaffar, Jade, additional, Westall, Glen, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie L., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2023
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