Inflammatory mechanisms involving neutrophils in chronic venous insufficiency of lower limbs

Bratisl Lek Listy. 2001;102(5):235-9.

Abstract

Background: It is supposed that an inflammatory reaction is one of the major factors responsible for the chronic venous insufficiency (CVI) of lower limbs which cause leg ulcers.

Objectives: The main objective of the present study was to determine the differences in the levels of typical inflammatory mediators and markers produced by neutrophils of patients with CVI and normal control subjects.

Subjects and methods: 26 patients with CVI and 39 clinically healthy subjects were included in the study. In peripheral neutrophils of both groups the production of superoxide, total reactive oxygen intermediates and activities of lysosomal enzymes were measured together with the expression of 8 adhesion molecules.

Results: Increased formation of superoxide by patient neutrophils and activities of elastase in both neutrophils and serum of patients were demonstrated. On the contrary, activities of myeloperoxidase and beta-D-glucuronidase were decreased in patient neutrophils. Comparing to control group adhesion molecules CD11b, CD18, CD31, CD49d, CD54 and CD62L were increased on the surface of patient neutrophils whereas no differences were observed in the expression of CD11a abd CD15.

Conclusion: The neutrophils of patients with CVI are primed and/or activated because they are able to release higher amount of superoxide, lysosomal enzymes and express elevated number of adhesion molecules. It may serve as one of the important evidences of an inflammatory mechanism involved in the pathogenesis of chronic venous insufficiency. (Tab. 3, Ref. 27.)

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Cell Adhesion Molecules / metabolism
  • Chronic Disease
  • Female
  • Glucuronidase / metabolism
  • Humans
  • Inflammation Mediators / metabolism*
  • Leg / blood supply*
  • Male
  • Middle Aged
  • Muramidase / metabolism
  • Neutrophils / metabolism*
  • Pancreatic Elastase / metabolism
  • Peroxidase / metabolism
  • Superoxides / metabolism
  • Venous Insufficiency / metabolism*

Substances

  • Cell Adhesion Molecules
  • Inflammation Mediators
  • Superoxides
  • Peroxidase
  • Muramidase
  • Glucuronidase
  • Pancreatic Elastase