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Polymorphonuclear cell derangements in type I diabetes.

D Tater1, B Tepaut, J P Bercovici

  • 1Unit of Diabetology, Centre Hospitalier Universitaire, Brest, France.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|December 1, 1987
PubMed
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Type I diabetes impairs polymorphonuclear cell function, except phagocytosis, impacting immune response. These neutrophil abnormalities persist regardless of infection or glycemic control.

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Type I diabetes mellitus is a chronic endocrine disorder characterized by hyperglycemia.
  • Polymorphonuclear cells (neutrophils) are critical components of the innate immune system, essential for combating infections.
  • Dysfunctional immune responses are frequently observed in diabetic patients, increasing susceptibility to infections.

Purpose of the Study:

  • To investigate polymorphonuclear cell (PMN) function in Type I diabetic subjects.
  • To assess the impact of diabetes on various PMN functions, including chemotaxis, phagocytosis, adherence, bactericidal activity, and NBT reduction.
  • To evaluate the role of Fc gamma receptor expression and immune complex interactions with PMNs in diabetes.

Main Methods:

  • Evaluated PMN functions (chemotaxis, phagocytosis, adherence, bactericidal activity, NBT reduction) in 58 Type I diabetic subjects and compared them to non-diabetic controls.

Related Experiment Videos

  • Enumerated Fc gamma receptor-bearing PMNs and the percentage of immune complexes containing PMNs.
  • Analyzed data in relation to glycemic levels and the presence of infections.

    • Main Results:

    • Most PMN functions were significantly decreased in Type I diabetics compared to controls, with the exception of phagocytosis.
    • Diabetic sera demonstrated reduced efficiency in supporting normal PMN functions (bactericidal activity, chemotactic index, phagocytosis).
    • Reduced percentage of Fc gamma receptor-bearing PMNs (70.1% vs 80.2%) and increased percentage of immune complexes containing PMNs (9.06% vs 4.75%) were observed in diabetics. These findings were independent of infection and glycemic control.

    Conclusions:

    • Type I diabetes is associated with significant impairments in polymorphonuclear cell function, potentially compromising the innate immune response.
    • The observed PMN abnormalities are not directly correlated with glycemic levels or the presence of infections.
    • These functional deficits in neutrophils may contribute to the increased infection risk in individuals with Type I diabetes.