Blood polymorphonuclear behavior in patients with ankylosing spondylitis

Area of Science:

• Immunology
• Rheumatology
• Cell Biology

Background:

• Ankylosing spondylitis (AS) is a chronic inflammatory disease.
• Polymorphonuclear leukocytes (PMNs) play a role in inflammation.
• Dysfunctional PMNs may contribute to AS pathogenesis.

Purpose of the Study:

• To investigate the oxidative metabolism and chemotaxis of PMNs in AS patients.
• To compare PMN function in AS patients versus healthy controls.
• To identify potential intrinsic PMN abnormalities in AS.

Main Methods:

• Collected PMNs from AS patients and healthy subjects.
• Assessed oxidative metabolism via oxygen consumption and superoxide anion release.
• Stimulated PMNs with opsonized zymosan, phorbol myristate acetate, and calcium ionophore (A 23187).
• Evaluated PMN chemotaxis using two parallel methods.

Main Results:

• PMNs from AS patients exhibited significantly lower responses to opsonized zymosan regarding oxygen consumption and superoxide anion release.
• No significant differences in oxidative metabolism were observed when PMNs were stimulated with phorbol myristate acetate or calcium ionophore.
• PMN chemotaxis remained unchanged in AS patients compared to controls.
• A seric factor was not implicated in the observed PMN dysfunction.

Conclusions:

• PMNs from AS patients display a specific defect in oxidative metabolism, particularly in response to immune complex-mediated stimuli like zymosan.
• The observed abnormality appears intrinsic to the PMNs, as chemotaxis and responses to other stimuli were unaffected.
• Further research is needed to fully characterize the intrinsic abnormality of PMNs in ankylosing spondylitis.