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Relationship between respiratory burst and adhesiveness capacity in elderly polymorphonuclear cells
C Tortorella1, A Ottolenghi, P Pugliese
1Medicina Interna, Istituto di Medicina Clinica, University of Bari Medical Faculty, Italy.
Mechanisms of Ageing and Development
|June 1, 1993
Summary
Immune cell function declines with age. Polymorphonuclear cell (PMN) activation shows reduced adherence and altered superoxide anion generation in the elderly, indicating an immune imbalance.
Area of Science:
- Immunology
- Gerontology
- Cellular Biology
Background:
- Polymorphonuclear cells (PMNs) are crucial for innate immunity.
- Aging is associated with immunosenescence, affecting immune cell function.
- Understanding age-related changes in PMN function is vital for immune health in the elderly.
Purpose of the Study:
- To investigate age-related alterations in Polymorphonuclear cell (PMN) activation.
- To assess PMN adherence and superoxide anion (O2-) generation in elderly individuals compared to younger controls.
- To explore the role of specific cell surface molecules in age-related PMN dysfunction.
Main Methods:
- Assessed PMN adherence to various substrates (nylon fibers, FCS-coated plates).
- Measured superoxide anion (O2-) generation in response to agonists like phorbol 12-myristate 13-acetate (PMA) and formyl-methionyl-leucine-phenylalanine (FMLP).
- Utilized monoclonal antibodies (anti-CD11b, anti-CD11c, anti-CD18) to investigate the role of integrins in PMN adhesion and function.
Main Results:
- PMNs from elderly donors showed normal PMA-stimulated O2- generation but reduced FMLP-stimulated respiratory burst.
- Aged individuals exhibited decreased PMN adherence to fetal calf serum (FCS)-coated surfaces.
- Adhering PMNs from the elderly produced more O2- than suspended cells, and antibody treatments revealed specific roles for CD18 in adhesion and O2- generation.
Conclusions:
- PMN-mediated functions are imbalanced in the elderly.
- Specific agonists reveal differential age-related defects in PMN activation.
- Integrin pathways, particularly involving CD18, play a role in age-associated PMN functional deficits.