Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.739968
Title: Streptococcus pneumoniae-stress hormone interactions
Author: Alghofaili, Fayez Abdullah
ISNI:       0000 0004 7231 800X
Awarding Body: University of Leicester
Current Institution: University of Leicester
Date of Award: 2018
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Abstract:
Streptococcus pneumoniae is one of the most important bacterial pathogens of humans causing a wide range of mild to life-threating diseases. It is also a commensal microorganism in the nasopharynx of up to 60% of people. Fundamental aspects of its ability for transition from colonisation to an infectious state as well as how bacterial-host interactions influence this process are largely unknown. In the field of microbial endocrinology, it has been well established in mainly Gram-negative bacteria that stress hormones such as norepinephrine epinephrine and dopamine play an essential role in determining the outcome of bacterial infections. This study successfully established the conditions to investigate S. pneumoniae-stress hormone interactions using modified serum-SAPI media. 13 mutants lacking two-component regulatory system and 4 two-component system fusion reporter strains were created, and examined for their role in S. pneumoniae-stress hormone interactions. This study demonstrated that S. pneumoniae is stress hormone responsive and has mechanisms to recognise and process host stress hormones by a transferrin-iron delivery mechanism, which evidence suggests might be mediated via the TCS09 system since hormone-induced growth and radiolabelled norepinephrine and Fe uptake were reduced in a ΔTCS09 mutant. In addition, the pneumococcal response to stress hormone exposure resulted in a change in cell-cell association from chains into diplococci and cell morphology by reducing cell size and the capsule. Furthermore, the pneumococcal exposure to norepinephrine also increased biofilm formation and significantly altered metabolism. The analysis of in vivo experiments indicated that a stress hormone encounter might trigger translocation from the nasopharynx into the lungs, which may enhance S. pneumoniae in its transition from commensal to pathogen. Therefore, the pneumococcal ability to respond to host stress signals may be key to its capacity to cause life-threatening pneumonia, septicaemia and meningitis.
Supervisor: Yesilkaya, Hasan ; Freestone, Primrose Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.739968  DOI: Not available
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