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Polymorphonuclear cell-mediated oxidative responsiveness in the elderly

C Tortorella1, E Jirillo, S Antonaci

  • 1Immunologia, University of Bari Medical School, Policlinico, 1-70124 Bari, Italy.

Archives of Gerontology and Geriatrics
|January 1, 1994
PubMed

Insights

Aging impairs polymorphonuclear cell (PMN) oxidative responses, particularly those triggered by formyl peptide (FMLP). This selective dysfunction in the elderly may involve membrane changes and reduced receptor expression, impacting immune defense.

Area of Science:

  • Immunology
  • Gerontology
  • Cellular Biology

Background:

  • Free radicals and toxic oxygen metabolites contribute to aging pathogenesis.
  • Activated polymorphonuclear cells (PMNs) release oxidants, potentially increasing with age.
  • Age-related decline in PMN function is a growing concern in geriatric health.

Purpose of the Study:

  • To investigate the mechanisms behind age-related impairment in PMN oxidative burst.
  • To differentiate between general PMN dysfunction and specific deficits in aging individuals.
  • To explore the role of membrane properties, receptor expression, and cell adhesion in PMN aging.

Main Methods:

  • Assessing PMN superoxide anion (O(2)()) generation in response to formyl peptide (FMLP) and phorbol 12-myristate 13-acetate (PMA).
  • Evaluating the impact of membrane microviscosity and cytoskeleton on FMLP receptor expression.
  • Examining the effect of lipopolysaccharide (LPS)-priming on PMN oxidative response.
  • Analyzing beta(2) integrin-dependent PMN adhesiveness and O(2)() production in aged cells.

Main Results:

  • PMN oxidative response to FMLP is impaired with age, unlike PMA-induced responses.
  • Reduced membrane microviscosity and decreased FMLP receptor expression are implicated in this deficit.
  • LPS-priming does not fully restore FMLP-induced PMN oxidative response.
  • While PMN adhesiveness shows age-related defects, adherent aged cells exhibit increased O(2)() production, suggesting prolonged release.

Conclusions:

  • Aging leads to a selective dysfunction in the oxidative metabolism of PMNs.
  • Mechanisms include altered membrane properties and reduced FMLP receptor expression.
  • These age-related PMN deficits may impact immune surveillance and response to infections in the elderly.

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