Dr Sj Sijie Shen is a researcher in respiratory and gastrointestinal tract diseases, with a major focus on the interaction between host immunity and microbiomes. He has a special interest in the role diet plays in immune responses and disease progression.
Dr Shen completed his Bachelor of Biomedical Sciences (Honours) at Monash University VIC (2014), examining the effect of fibre and short-chain fatty acids in Allergic Bronchopulmonary Aspergillosis and Eosinophilic Oesophagitis.
He completed his PhD at Monash Medical Centre/Monash Univervisty VIC (2019) examining the interplay between the gut microbiome and neutrophils in a mouse model of colitis.
Member of ASI and TSANZ.
Tavel award to the International Congress of Immuology 2016.
Oral presentations at national and international conferences, including World Congress for Microcirculation 2018 (Canada), VIIN Young Investigators Symposium (Victoria), and for Day of Immunology 2016 (Victoria).
Can supervise: YES
- Severe asthma
- Lung cancer
- Intravital microscopy
Donovan, C, Liu, G, Shen, S, Marshall, J, Kim, R, Alamao, CA, Budden, KF, Choi, JP, Kohonen-Corish, M, El-Omar, EM, Yang, IA & Hansbro, P 2020, 'The role of microbiome and NLRP3 inflammasome in the gut and the lung', Journal of Leukocyte Biology, vol. accepted 4.7.20.
Galvao, I, Kim, RY, Shen, S, Budden, KF, Vieira, AT & Hansbro, PM 2020, 'Emerging therapeutic targets and preclinical models for severe asthma', EXPERT OPINION ON THERAPEUTIC TARGETS.View/Download from: Publisher's site
Nucera, F, Lo Bello, F, Shen, SS, Ruggeri, P, Coppolino, I, Di Stefano, A, Stellato, C, Casolaro, V, Hansbro, PM, Adcock, IM & Caramori, G 2020, 'Role of Atypical Chemokines and Chemokine Receptors Pathways In the Pathogenesis of COPD', Current medicinal chemistry.View/Download from: Publisher's site
Chronic obstructive pulmonary disease (COPD) represents a heightened inflammatory response in the lung resulting generally from tobacco smoking-induced recruitment and activation of inflammatory cells and/or activation of lower airway structural cells. Several mediators can modulate activation and recruitment of these cells, particularly those belonging to the chemokines (conventional and atypical) family. There is emerging evidence for complex roles of atypical chemokines and their receptors [such as high mobility group box 1 (HMGB1), antimicrobial peptides, receptor for advanced glycosylation end product (RAGE) or toll-like receptors (TLRs)] in the pathogenesis of COPD, both in the stable disease and during exacerbations. Modulators of these pathways represent potential novel therapies for COPD and many are now in pre-clinical development. Inhibition of only a single atypical chemokine or receptor may not block inflammatory processes, be-cause there is redundancy in this network. However, there are many animal studies that encourage studies for modulating the atypical chemokine network in COPD. Thus, few pharmaceutical companies maintain a significant interest in developing agents that target these molecules as potential anti-inflammatory drugs. Antibody-based (biological) and small molecule drug (SMD)-based therapies targeting atypical chemokines and/or their receptors are mostly at the preclinical stage and their progression to clinical trials is eagerly awaited. These agents will most likely enhance our knowledge about the role of a typical chemokines in COPD pathophysiology and thereby improve COPD management.
Wen, SW, Shim, R, Ho, L, Wanrooy, BJ, Srikhanta, YN, Prame Kumar, K, Nicholls, AJ, Shen, SJ, Sepehrizadeh, T, de Veer, M, Srikanth, VK, Ma, H, Phan, TG, Lyras, D & Wong, CHY 2019, 'Advanced age promotes colonic dysfunction and gut-derived lung infection after stroke.', Aging cell, vol. 18, no. 5.View/Download from: Publisher's site
Bacterial infection a leading cause of death among patients with stroke, with elderly patients often presenting with more debilitating outcomes. The findings from our retrospective study, supported by previous clinical reports, showed that increasing age is an early predictor for developing fatal infectious complications after stroke. However, exactly how and why older individuals are more susceptible to infection after stroke remains unclear. Using a mouse model of transient ischaemic stroke, we demonstrate that older mice (>12 months) present with greater spontaneous bacterial lung infections compared to their younger counterparts (7-10 weeks) after stroke. Importantly, we provide evidence that older poststroke mice exhibited elevated intestinal inflammation and disruption in gut barriers critical in maintaining colonic integrity following stroke, including reduced expression of mucin and tight junction proteins. In addition, our data support the notion that the localized pro-inflammatory microenvironment driven by increased tumour necrosis factor-α production in the colon of older mice facilitates the translocation and dissemination of orally inoculated bacteria to the lung following stroke onset. Therefore, findings of this study demonstrate that exacerbated dysfunction of the intestinal barrier in advanced age promotes translocation of gut-derived bacteria and contributes to the increased risk to poststroke bacterial infection.
Shen, S, Kumar, KP, Stanley, D, Moore, RJ, Thi, THV, Wen, SW, Hickey, MJ & Wong, CHY 2018, 'Invariant Natural Killer T Cells Shape the Gut Microbiota and Regulate Neutrophil Recruitment and Function During Intestinal Inflammation', FRONTIERS IN IMMUNOLOGY, vol. 9.View/Download from: Publisher's site
Thorburn, AN, McKenzie, CI, Shen, S, Stanley, D, Macia, L, Mason, LJ, Roberts, LK, Wong, CHY, Shim, R, Robert, R, Chevalier, N, Tan, JK, Marino, E, Moore, RJ, Wong, L, McConville, MJ, Tull, DL, Wood, LG, Murphy, VE, Mattes, J, Gibson, PG & Mackay, CR 2015, 'Evidence that asthma is a developmental origin disease influenced by maternal diet and bacterial metabolites', NATURE COMMUNICATIONS, vol. 6.View/Download from: Publisher's site
© 2020 John Wiley & Sons Ltd Due to the rapid development of the cloud computing environment, it is widely accepted that cloud servers are important for users to improve work efficiency. Users need to know servers' capabilities and make optimal decisions on selecting the best available servers for users' tasks. We consider the process of learning servers' capabilities by users as a multiagent reinforcement learning process. The learning speed and efficiency in reinforcement learning can be improved by sharing the learning experience among learning agents which is defined as advising. However, existing advising frameworks are limited by the requirement that during advising all learning agents in a reinforcement learning environment must have exactly the same actions. To address the above limitation, this article proposes a novel differentially private advising framework for multiagent reinforcement learning. Our proposed approach can significantly improve the application of conventional advising frameworks when agents have one different action. The approach can also widen the applicable field of advising and speed up reinforcement learning by triggering more potential advising processes among agents with different actions.