Dr Kendle Michelle Maslowski PhD

Dr Kendle Michelle Maslowski

Institute of Immunology and Immunotherapy
Birmingham Fellow

Contact details

Address
Institute of Immunology and Immunotherapy
University of Birmingham
Edgbaston
Birmingham
B15 2TT
UK

Kendle is a Birmingham Fellow working across the Institutes of Immunology and Immunotherapy (III), and Metabolism and Systems Research (IMSR).

Research in Kendle’s lab is focussed on understanding innate immune pathways in intestinal epithelial cells and their roles in fighting infection and cancer development.

Qualifications

  • PhD Medicine 2011
  • BSc Hons 2006
  • BSc 2005

Biography

Kendle qualified with a BSc (Hons) in Molecular Biology from Murdoch University, Western Australia, in 2006. She then went on to study her PhD with Charles Mackay at the Garvan Institute in Sydney, Australia, where she published seminal work on a diet­­-gut microbiota-immune regulation axis.

In 2011, Kendle joined the laboratory of Jurg Tschopp in Lausanne, Switzerland, where she studied the role of epithelial-intrinsic NAIPs in Salmonella infection and cancer suppression. Following this, Kendle was awarded a Special Postdoctoral Fellowship at the RIKEN in Yokohama, Japan, where she joined the Laboratory of Hiroshi Ohno. Here she studied mechanisms of attenuated Salmonella therapy in colon cancer.

In 2017, Kendle was awarded a Birmingham Fellowship to establish her own laboratory at the University of Birmingham.

Postgraduate supervision

For any doctoral research enquiries, please email:

k.m.maslowski@bham.ac.uk

Research

Kendle’s research is focussed on understanding epithelial innate immune pathways, particularly involving the NLR apoptosis inhibitory proteins. She aims to dissect pathways that are involved in protecting the epithelium against pathogenic infection and tumourigenesis. Key areas of research: 

Epithelial-intrinsic NAIP pathways

NAIPs are well-described to form an inflammasome in innate immune cells such as macrophages. While NAIPs do detect intracellular Salmonella in enterocytes, inflammasome formation appears to be different to that in macrophages. Additionally NAIPs were found to supress tumourigenesis in an inflammasome-independent manner. Therefore, an major aim is to better understand NAIPs molecular pathways in the epithelium. This will be achieved using novel colon organoid in vitro cultures, coupled with molecular biology techniques and mass spectrometry to understand NAIPs binding partners. These findings will be related back to NAIPs function in tumour suppression and Salmonella inhibition.

Mechanisms of attenuated Salmonella cancer therapy

Kendle is interested in understanding how infection of colorectal tumours with attenuated Salmonella leads to tumour regression. She is combining understanding of epithelial immunity with tecniques such as metabolomics to unpick the mechanisms. Future attemps to deliver bacteria with specific cargo will be tested. And this therapy and mechanisms will be tested in human tumour organoid cultures.

Publications

Maslowski K., Kanaya T., Ohno H. (2016) Innate immune pathways of the intestinal epithelium protecting against infection and tumourigenesis. Clinical Immunol. & Allergol. 66(3), 294-300. (review in Japanese).

Sellin ME, Maslowski KM, Maloy KJ, Hardt WD. (2015) Inflammasomes of the intestinal epithelium. Trends Immunol. 36(8), 442-50. http://www.ncbi.nlm.nih.gov/pubmed/26166583   

Vieira, A. T., Macia, L., Galvao, I., Martins, F. S., Canesso, M. C., Amaral, F. A., Garcia, C. C., Maslowski, K. M., De Leon, E., Shim, D., Nicoli, J. R., Harper, J. L., Teixeira, M. M. and Mackay, C. R. (2015) A Role for Gut Microbiota and the Metabolite-Sensing Receptor GPR43 in a Murine Model of Gout. Arthritis Rheumatol. 67(6). 1646-56. http://www.ncbi.nlm.nih.gov/pubmed/25914377

Allam, R., Maillard, M. H., Chennupati, V., Bega, H., Tardivel, A., Yu, C. W., Velin, D., Schneider, P., and Maslowski, K. M.* (2015). Epithelial NAIPs protect against colonic tumorigenesis. J. Exp. Med. 212(3), 369-383 https://www.ncbi.nlm.nih.gov/pubmed/25732303

Sellin, M. E., Muller, A. A., Felmy, B., Dolowschiak, T., Diard, M., Tardivel, A., Maslowski, K. M., and Hardt, W. D. (2014). Epithelium-intrinsic NAIP/NLRC4 inflammasome drives infected enterocyte expulsion to restrict Salmonella replication in the intestinal mucosa. Cell Host Microbe 16, 237-248. https://www.ncbi.nlm.nih.gov/pubmed/25121751

Scott, C., Bonner, J., Min, D., Boughton, P., Stokes, R., Cha, K. M., Walters, S. N., Maslowski, K., Sierro, F., Grey, S. T., et al. (2014). Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing. Am J Physiol Cell Physiol 307, C349-357. http://www.ncbi.nlm.nih.gov/pubmed/24990649

Zaiss, M. M., Maslowski, K. M., Mosconi, I., Guenat, N., Marsland, B. J., and Harris, N. L. (2013). IL-1beta suppresses innate IL-25 and IL-33 production and maintains helminth chronicity. PLoS Pathog 9, e1003531. http://www.ncbi.nlm.nih.gov/pubmed/23935505

Michallet, M. C., Rota, G., Maslowski, K., and Guarda, G. (2013). Innate receptors for adaptive immunity. Curr Opin Microbiol 16, 296-302. http://www.ncbi.nlm.nih.gov/pubmed/23659869

Macia, L., Thorburn, A. N., Binge, L. C., Marino, E., Rogers, K. E., Maslowski, K. M., Vieira, A. T., Kranich, J., and Mackay, C. R. (2012). Microbial influences on epithelial integrity and immune function as a basis for inflammatory diseases. Immunol Rev 245, 164-176. http://www.ncbi.nlm.nih.gov/pubmed/22168419

Kranich, J., Maslowski, K. M., and Mackay, C. R. (2011). Commensal flora and the regulation of inflammatory and autoimmune responses. Semin Immunol 23, 139-145. http://www.ncbi.nlm.nih.gov/pubmed/21292499

Maslowski, K. M., and Mackay, C. R. (2010). Diet, gut microbiota and immune responses. Nat Immunol 12, 5-9. http://www.ncbi.nlm.nih.gov/pubmed/21169997

Maslowski, K. M., Vieira, A. T., Ng, A., Kranich, J., Sierro, F., Yu, D., Schilter, H. C., Rolph, M. S., Mackay, F., Artis, D., et al. (2009). Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature 461, 1282-1286. https://www.ncbi.nlm.nih.gov/pubmed/19865172