The Final ImResFun Scientific Conference of the EC-funded Marie-Curie Initial Training Network ImResFun is now announced.

Publication: Candidalysin is a fungal peptide toxin critical for mucosal infection

ITN Practical Course "C2a", Barcelona, Spain (May 10-15, 2015)

ITN Meeting, La Colle sur Loup, France (May 16, 2015)

HPF2015, La Colle sur Loup, France (May 16-22, 2015)

ITN Practical Course "S3" & "C3", Madrid, Spain (July 6-10, 2015)

ITN Mid-Term Review Meeting, Vienna, Austria (November 3, 2015)

ITN Practical Course "S5" & "C5", Tübingen, Germany (May 9-11, 2016)

ITN Lecture Course "S4" & "C4", Szeged, Hungary (July 2-8, 2016)

ITN Practical Course "S6" & "C6", Göttingen, Germany (October 26-28, 2016)

ITN Symposium "S7" & Final Consortium Meeting, Innsbruck, Austria (January 28-30, 2017)


Name & Address

Julian Naglik Portrait

Julian NaglikReader in Mucosal Immunology and Fungal Pathogenesis
King’s College London
Clinical and Diagnostic Science Group
Room 2.67, Floor 2, Hodgkin Building, Guy’s Campus
London, SE1 1UL, United Kingdom
Phone: +44-20-7848-6123 FAX: +44-20-7848-6210
Web: &

ESR-KCL Project: (Start November/December 2013)

Mucosal Candida infections – from commensal to pathogen

The ESR will investigate how epithelial cells discriminate between C. albicans yeast and hyphal forms, identifying novel receptors that mediate fungal recognition through targeted proteomics and chemical inhibition. In vitro epithelial infection models and in vivo systems will be utilised to determine the importance of these recognition mechanisms in inducing protective innate/adaptive immune responses.

Main Research Interests

Our research interests focus on C. albicans infections of human mucosal tissues and specifically how oral epithelial cells recognise C. albicans and orchestrate protective immune responses against this fungus. We have shown that epithelial cells orchestrate the innate response against C. albicans via NF-kB, MAPK and PI3K signalling pathways. NF-kB activation is independent of morphology (Candida forms yeast and hyphae) and results from generic recognition of fungal moieties present on all Candida spp. The MAPK network is activated in a bi-phasic manner, which is hyphal- and dose-dependent. This ‘danger response’ constitutes activation of the MAPK phosphatase MKP-1 and the transcription factor c-Fos that results in a pro-inflammatory response, which leads to a ‘protective’ host phenotype through the recruitment of polymorphonuclear cells and epithelial TLR4. The PI3K pathway is involved in protecting epithelial cells from fungal-induced damaged. Our current work aims to (i) identify the C. albicans hyphal moieties that activate the MAPK and PI3K pathways, (ii) identify the epithelial receptors that mediate hyphal recognition, (iii) determine the importance of epithelial inflammasome activation in mediating protective innate immunity and (iv) ascertain the importance of epithelial cells in orchestrating protective adaptive immunity. The major goal is to understand how human mucosal surfaces discriminate between commensal and pathogenic states of C. albicans and to identify the recognition mechanisms that induce protective innate/adaptive immune responses. This will significantly advance our understanding of how human mucosal surfaces control these important fungal pathogens.

Selected Recent Publications

Moyes DL Runglall M, Murciano C, Shen C, Nayar D, Thavaraj S, Kohli A, Islam A, Mora-Montes M, Challacombe SJ, and Naglik JR (2010). A biphasic innate immune MAPK response discriminates between the yeast and hyphal forms of Candida albicans in Epithelial Cells. Cell Host and Microbe 8 (3), 225-35.

Weindl G, Naglik JR, Kaesler S, Biedermann T, Hube B, Korting HC and Schaller M (2007). Epithelial cells establish direct antifungal defense through Toll-like receptor 4-mediated signaling. Journal of Clinical Investigation 117(12): 3664-3672.

Moyes DL, Murciano C, Runglall M, Islam A, Thavaraj S and Naglik JR (2011). Candida albicans yeast and hyphae are discriminated by MAPK signalling in vaginal epithelial cells. PLoS One 6 (11), e26580