Centre for Inflammation Research

Dr Chengcan Yao

Chengcan Yao's lab studies the roles of bioactive lipids in modulation of immunity and inflammatory diseases in barrier tissues.

Dr Chengcan Yao

Reader / MRC Career Development Award (CDA ) Fellow

  • Centre for Inflammation Research

Contact details

Group Members

  • Fiona Cunningham - CSO Clinical Academic Training Fellowship
  • Jemma Milburn – Post-Doctoral Research Associate
  • Meenakshi Anilkumar – MSc student


Barrier tissues, such as intestine, lung and skin, directly and continuously interact with the outside environment, thus require specialized immune cells to properly respond to external stimuli like injury and infections. During this process, cells at the barrier tissue produce various mediators including bioactive lipids such as eicosanoids, which play critical roles in modulating immune cell functions. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, which block biological synthesis of eicosanoids, are widely used to treat numerous conditions from inflammation (e.g., pain and fever) to cancers but can also lead to adverse effects in multiple organs including garstrointestinal bleeding and asthma exaerbation. This indicates that eicosanoids can have both harmful and beneficial functions in the barrier tissues.

Research Overview

Our research is aiming to illustrate the underlying cellular and molecular mechanisms for how lipid mediators modulate the barrier immune system, to develop improved treatments for complex degenerative and inflammatory conditions at the barrier sites. We are currently focusing on the classic inflammatory eicosanoid - prostaglandin E2 (PGE2).

  1. Lipid mediators in the communications between the host immune system and the commensal microbiota in healthy and diseased gut

Eicosanoids, especially PGE2, are well-known to be homeostatic lipid mediators in the gut, where they maintain the epithelial integrity and protect against acute injury of the gastrointestinal wall. This underscores the adverse effects of NSAIDs in the gastrointestinal tract. The protective effects of PGE2 are achieved through binding to its receptors (mainly the EP4 receptor) on various types of cells including epithelial cells, mononuclear phagocytes (MNPs) and group 3 innate lymphoid cells (ILC3s). For example, we have recently identified that PGE2 stimulates ILC3s to produce the reparative cytokine IL-22 to maintain the epithelial homeostasis (Duffin et al. 2016 Science). On the other side, as a typical inflammatory factor, PGE2 restrains intestinal regulatory T cell (Treg) responses through indirect actions on gut microbes and MNPs, resulting in reduced production of Treg-facilitating type I interferons (Crittenden et al. 2021 Science Advances) as well as direct actions on T cells by down-regulation of TGF-b signalling (Goepp et al. 2022 Immunology).

Simultaneously, the roles of eicosanoids, especially their actions on immune cells and the gut microbiota during intestinal inflammation such as Crohn’s disease, are unclear, despite the work of ourselves and others suggesting a role of PGE2-EP4 signalling in T cells in the development of intestinal effector T cells (Teff) (e.g., Th1 cells) during mucosal inflammation (Yao et al. 2013 Nat Comm). Furthermore, aspirin and other NSAIDs have long been proposed to be beneficial for preventing and/or reducing bowel cancers by evidence from many animal and human epidemiological studies. However, the exact immune mechanisms underpinning eicosanoid facilitation of the development of bowel cancer remain to be fully elucidated.


   2. Lipid-immune interplay in inflammatory lung diseases

Eicosanoids are bioactive lipid mediators that play critical roles in regulation of lung immune responses and allergic diseases. Use of NSAIDs such as aspirin and ibuprofen can cause lung damage and exacerbation of allergic responses, although the underlying immune mechanisms are not clear. Our recent studies indicate that PGE2 limits allergic lung inflammation through inhibiting group 2 innate lymphoid cells (ILC2s) (Robb et al. 2022 Allergy) and protects against acute lung injury through promoting reparative group 3 innate lymphoid cell (ILC3) (Felton et al. 2018 Thorax). We are currently investigating the role of PGE2 regulation of immune responses in human lung diseases such as asthma.


   3. Lipid-immune interplay in skin inflammation

Lesional and non-lesional skin from patients with eczema and psoriasis have increased expression of eicosanoids such as PGE2 and their receptor. Our work has demonstrated that PGE2 directly acts on T cells to promote various subsets of effector T cells such as Th1, Th17 and Th22 cells, facilitating T cell-mediated skin inflammation in different animal models (Robb et al. J Allergy Clin Immunol 2018; Lee et al, J Allergy Clin Immunol 2019). We now work on whether this mechanism similarly happens in human skin diseases.

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Biographical Profile

Chengcan Yao received his PhD in Biomedical Science from Kyoto University at 2010. He then did his post-doc with Professor Shuh Narumiya at Kyoto University as a JSPS (Japan Society for the Promotion of Science) Postdoctoral Fellow for Overseas Researchers. From 2013, Chengcan established his independent research at the Centre for Inflammation Research (CIR) in the University of Edinburgh as a Chancellor's Fellowship.

Honours and Awards

  • Host and local organiser of the 9th European Workshop for Lipid Mediators (9EWLM), 2024
  • Elected Fellow of the British Pharmacological Society, 2022
  • Board Member of the European Society of Lipid Mediators, 2020
  • Member of the Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR) Prostaglandin, 2019
  • MRC Career Development Fellowship, 2018-2023
  • CRUK Cancer Immunology Project Award, 2018-2021
  • International Eicosanoid Research Foundation (ERF) Young Investigator Award, 2015
  • Chancellor's Fellowship, The University of Edinburgh, 2013-2018
  • Japan Society for the Promotion of Science Research Fellow, 2010-2012


Post-doctoral Research associates
  • Marie Goepp (Resolution Therapeutics)
  • Calum Robb (ThermoFisher Scientific)
PhD students
  • Siobhan Crittenden (Cambridge Research Biochemicals)
  • Jack McGeown (Queen’s University Belfast)
MSc students
  • Fiona Cunningham (UoE/NHS), Matthew McIlorum (NHS), Cameron Elder, Jiahao Luo, Hatti Yao (University of Glasgow), Tianjiao Xu, Sarah Mohd Noor, Tom Collings, Yuhang Zheng
BSc students
  • Ashleigh Cheyne, Amil Mair (NHS), Chris Brown (NHS), Aleksandra Prochera, Alex Adima (NHS), Jayne Murdock, Hatti Yao, James Ettles, Privjyot Jheeta (NHS), Annie Whelan, Noah Slinn, Zara Khan, Osher Lee, Yijia Dong, Roisin MacDonald


  • Professor Mark Arends (University of Edinburgh)
  • Dr Tracey Bradshaw (NHS Lothian)
  • Professor Richard Breyer (Vanderbilt University)
  • Dr Farhat Din (CRUK Edinburgh Centre)
  • Professor Konstantinos Gerasimidis (University of Glasgow)
  • Professor Rick Maizels (University of Glasgow)
  • Dr Henry McSorley (University of Dundee)
  • Professor Damian Mole (University of Edinburgh)
  • Professor Shuh Narumiya (Kyoto University)
  • Professor Valerie O'Donnell (Cardiff University)
  • Professor Adriano Rossi (University of Edinburgh)
  • Professor Owen Sansom (Beatson Institute for Cancer Research)
  • Professor Jack Satsangi (University of Oxford)
  • Professor Jürgen Schwarze (University of Edinburgh)
  • Dr Richard Weller (University of Edinburgh)
  • Dr You Zhou (Cardiff University)

Sources of Funding

  • Medical Research Council
  • Cancer Research UK
  • Chief Scientist Office

More information on funding at Chengcan Yao's Research Explorer profile.