Dr Hasan Yesilkaya

Associate ProfessorHasan Yesilkaya portrait

Contact Details

Department of Respiratory Sciences
College of Life Sciences
Room 217c, Maurice Shock Building
University of Leicester, University Road, Leicester, LE1 7RH, UK

Tel: +44 (0)116 2231401
Email: hy3@le.ac.uk


Microbes encounter fluctuating nutrient and physical environments in host tissues. In this dynamic milieu, bacteria should be able to obtain the host nutrients and metabolise them for efficient replication, and virulence. However, our knowledge of how microbes maintain their survival in vivo is very limited. I have been studying microbial physiology and metabolic adaptation using Streptococcus pneumoniae as a model organism to understand microbial in host survival and virulence. My ultimate research goals are to define critical metabolic microbial networks associated with virulence in different host niches and target these pathways pharmaceutically. The particular topics I study include:

  • mechanisms by which microbes cleave and metabolise host-derived nutrients
  • the impact of genetic and environmental factors on microbial colonisation and virulence
  • the role of quorum sensing systems on pneumococcal physiology and in host survival.


Selected publications

Aggarwal SD, Yesilkaya H, Dawid S, Hiller NL. The pneumococcal social network. PLoS Pathog. 2020 Oct 29;16(10):e1008931.

Najmuldeen H, Alghamdi R, Alghofaili F, Yesilkaya H. Functional assessment of microbial superoxide dismutase isozymes suggests a differential role for each isozyme. Free Radic Biol Med. 2019 Apr;134:215-228.

Eutsey R, West-Roberts J,  Domenech A, Xu W, Abdullah IT, Mitchell AP, Veening JW, Yesilkaya H, Hiller NL. Function of BriC peptide in the pneumococcal competence and virulence portfolio. PLoS Pathog. 2018 Oct 11;14(10):e1007328.

Glanville DG, Han L, Maule AF, Woodacre A, Thanki D, Abdullah IT, Morrissey JA, Clarke TB, Yesilkaya H, Silvaggi NR, Ulijasz AT. RitR is an archetype for a novel family of redox sensors in the streptococci that has evolved from two- component response regulators and is required for pneumococcal colonization. PLoS Pathog. 2018 May 11;14(5):e1007052.

Zhi X, Abdullah IT, Gazioglu O, Manzoor I, Shafeeq S, Kuipers OP, Hiller NL, Andrew PW, Yesilkaya H. Rgg-Shp regulators are important for pneumococcal colonization and invasion through their effect on mannose utilization and capsule synthesis. Sci Rep. 2018 Apr 23;8(1):6369.

Motib A, Guerreiro A, Al-Bayati F, Piletska E, Manzoor I, Shafeeq S, Kadam A, Kuipers O, Hiller L, Cowen T, Piletsky S, Andrew PW, Yesilkaya H. Modulation of Quorum Sensing in a Gram-Positive Pathogen by Linear Molecularly Imprinted Polymers with Anti-infective Properties. Angew Chem Int Ed Engl. 2017 Dec 22;56(52):16555-16558.

Hajaj B, Yesilkaya H, Shafeeq S, Zhi X, Benisty R, Tchalah S, Kuipers OP, Porat N. CodY Regulates Thiol Peroxidase Expression as Part of the Pneumococcal Defense Mechanism against H2O2 Stress. Front Cell Infect Microbiol. 2017 May 24;7:210.

Kadam A, Eutsey RA, Rosch J, Miao X, Longwell M, Xu W, Woolford CA, Hillman T, Motib AS, Yesilkaya H, Mitchell AP, Hiller NL. Promiscuous signaling by a regulatory system unique to the pandemic PMEN1 pneumococcal lineage. PLoS Pathog. 2017 May 18;13(5):e1006339.

Kahya HF, Andrew PW, Yesilkaya H. Deacetylation of sialic acid by esterases potentiates pneumococcal neuraminidase activity for mucin utilization, colonization and virulence. PLoS Pathog. 2017 Mar 3;13(3):e1006263.

Paixão L, Oliveira J, Veríssimo A, Vinga S, Lourenço EC, Ventura MR, Kjos M, Veening JW, Fernandes VE, Andrew PW, Yesilkaya H, Neves AR. Host glycan sugar- specific pathways in Streptococcus pneumoniae: galactose as a key sugar in colonisation and infection [corrected]. PLoS One. 2015 Mar 31;10(3):e0121042.

Additional Publications


I am a Fellow of the Higher Education Academy. I am involved in teaching undergraduate and postgraduate microbiology modules.


Topics available for supervision

The impact of in vivo derived sugars on bacterial physiology and virulence.

Oxidative stress response of pathogenic bacteria.

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