Inhibition of human polymorphonuclear leukocytes phagocytosis and protein-kinase-C activity by low pH concentrations

P Courtois1, M Pourtois, A Rerren

  • 1Laboratoire de Stomatologie, Faculté de Médecine, Université Libre de Bruxelles, Belgique.

Journal De Biologie Buccale
|December 1, 1987
PubMed

Insights

Periodontal disease may be linked to decreased pH and succinic acid. These factors inhibit polymorphonuclear (PMN) leukocyte function, impacting the body's defense mechanisms against chronic periodontitis.

Area of Science:

  • Immunology
  • Oral Biology
  • Biochemistry

Background:

  • Periodontal disease involves inflammation and tissue destruction.
  • Polymorphonuclear (PMN) leukocytes are crucial for innate immunity in the oral cavity.
  • The role of local environmental factors in periodontitis pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the functional status of PMN leukocytes in patients with periodontal disease.
  • To assess the impact of succinic acid and low pH on PMN leukocyte function.
  • To explore the potential role of these factors in the pathogenesis of chronic periodontitis.

Main Methods:

  • Collected PMN leukocytes from blood of periodontitis patients and healthy individuals.
  • Assessed PMN function using chemiluminescence, superoxide generation, degranulation, lactoferrin, myeloperoxidase, and protein-kinase-C activity.
  • Incubated PMN leukocytes with succinic acid and adjusted pH to 5.5.

Main Results:

  • No significant differences in PMN function between periodontitis patients and healthy controls.
  • Succinic acid severely inhibited PMN phagocytic ability (light emission and superoxide production).
  • Protein-kinase-C activity in PMN leukocytes decreased significantly at pH 5.5.

Conclusions:

  • Decreased pH and succinic acid in crevicular fluid may contribute to chronic periodontitis.
  • These factors can impair PMN leukocyte function, compromising host defense.
  • Further research is warranted to elucidate the precise mechanisms involved in periodontitis pathogenesis.

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