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The effect of age on neutrophil function and apoptosis: Role of superoxide anion and PKC isoenzymes

Reference	SAG09987
Principal Investigator / Supervisor	Professor Janet Lord
Co-Investigators / Co-Supervisors
Institution	University of Birmingham
Department	Medical Sciences - Medicine
Funding type	Research
Value (£)	154,834
Status	Completed
Type	Research Grant
Start date	01/10/1998
End date	01/10/2001
Duration	36 months

Abstract

Neutrophils from aged subjects show reduced phagocytosis and superoxide (O2-) generation response to E. coli. Neutrophilis are short-lived cells and the proliferation and differentiation capacity of granulocypte precursors does not decline with age. However, neutrophil functions do decline as neutrophils age in vivo and die by apoptosis. In other cells, apoptosis is known to decline with age leading to accumulation of senescent cells. We will test 2 hypotheses to explain reduced neutrophil function in the aged: 1) that neutrophils produced de novo have reduced function, and 2) that apotosis is delayed in neutrophils, resulting in a greater percentage of senescent cells. We will determine the role of O2- generation and altered signalling through PKC in neutrophil senescence and evaluate the ability of IL8, GM-CSF and butyrate to improve neutrophil response.

Summary

unavailable

Committee	Closed Committee - Genes & Developmental Biology (GDB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	Initiative on Science of Ageing (SAG) [1998]
Funding Scheme	X – not Funded via a specific Funding Scheme

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