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Do Altered host-microbial interactions promote oral inflammation during ageing?


Project Description

As we age, the systems of our bodies become less able to function; rendering people increasingly infirm. Ageing affects our immune system, impeding our ability to both fight infection and maintain tolerance. At barrier sites, such as the gut and oral barrier, this is a particular problem. The immune system at these barriers is delicately balanced; protecting against pathogens yet also distinguishing these invaders from the commensal-bacterial communities inhabiting these sites. To achieve this, immune responses at barrier sites are carefully tuned to their commensal partners and a successful host-microbe dialogue is established. Maintaining this balance becomes difficult as we age.

The influence of age on oral bacterial communities is minimally explored and how these evolving communities tune immune function is unknown. This is an oversight, as advancing age is accompanied by failure of oral barrier immune-homeostasis, resulting in increased incidence and severity of oral inflammation, particularly periodontitis. Critically, periodontitis is a risk factor for multiple disorders promoting unhealthy ageing, including cardiovascular disease and diabetes. Therefore, elucidating factors driving loss of oral barrier immune-homeostasis and development of inflammation is urgently required.

We hypothesize that an altered host-microbe dialogue promotes dysregulation of oral barrier immune responses with age. This project will outline how oral bacterial communities are remodelled during ageing and, importantly, the influence of this altered bacterial community on oral barrier immune functions. Collectively this work will further our understanding of how oral barrier inflammation arises with age, promoting development of therapeutics to reinforce oral barrier immune-homeostasis across a life-course.

Funding Notes

This project has a Band 3 fee. Details of our different fee bands can be found on our website (View Website). For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (View Website).

Informal enquiries may be made directly to the primary supervisor.

References

1) Moutsopoulos N.M., et al., Defective neutrophil recruitment in leukocyte adhesion deficient type 1 disease causes local IL-17-driven inflammatory bone loss. Sci Transl Med. 2014. 6(229):229ra40

2) Eskan M.A., et al., The leukocyte integrin antagonist Del-1 inhibits IL-17 mediated inflammatory bone loss. Nat Imm. 2012. 13, 465-473.

3) Hajishengallis G., et al., Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement. Cell Host and Microbe. 2011. 10(5). 497-506.

4) Claesson, M.J., et al., Gut microbiota composition correlates with diet and health in the elderly. Nature, 2012. 488(7410): p. 178-84.

5) Zanvit P., et al., Antibiotics in neonatal life increases murine susceptibility to experimental psoriasis. Nat Commun. 2015. 6(8424).

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