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Defective polymorphonuclear leukocyte metabolism and function in canine cyclic neutropenia
Abstract:
Humans and grey collie dogs with cyclic neutropenia are known to suffer from an increased rate of bacterial infection. Because of the previously described microanatomic abnormalities of lysosome formation found in the polymorphonuclear leukocytes (PMNs) of dogs with canine cyclic neutropenia, studies of these cells were undertaken. PMNs from grey collie dogs were found to have significant metabolic and functional abnormalities when compared with normal collie PMNs. These included abnormally increased postphagocytic C1-glucose oxidation, decreased iodination of trichloroacetic acid-precipitable protein in the resting and phagocytizing state, decreased levels of intracellular myeloperoxidase,and a bactericidal defect against a variety of bacteria. Phagocytosis was normal. These abnormalities appear to differ from those previously described in the PMNs of patients with chronic granulomatous disease of childhood and the Chediak-Higashi syndrome and more closely resemble those seen in hereditary myeloperoxidase deficiency. Thus, the studies reported here demonstrate defective PMN function in a disease state previously believed to be a model only of periodic hematopoiesis.
Insights
Cyclic neutropenia in grey collie dogs causes polymorphonuclear leukocyte (PMN) dysfunction, leading to increased bacterial infections. These PMN defects, including impaired bacterial killing, resemble hereditary myeloperoxidase deficiency.
Area of Science:
- Immunology
- Hematology
- Canine Pathology
Background:
- Cyclic neutropenia in grey collie dogs is associated with recurrent bacterial infections.
- Previous studies noted lysosome formation abnormalities in canine cyclic neutropenia polymorphonuclear leukocytes (PMNs).
Purpose of the Study:
- To investigate the metabolic and functional characteristics of PMNs from grey collie dogs with cyclic neutropenia.
- To compare these PMN abnormalities with known human neutrophil disorders.
Main Methods:
- Analysis of PMN metabolic functions, including C1-glucose oxidation and protein iodination.
- Assessment of intracellular myeloperoxidase levels and bactericidal activity.
- Comparison of PMN functional defects with chronic granulomatous disease and Chediak-Higashi syndrome.
Main Results:
- PMNs from grey collie dogs exhibited increased postphagocytic C1-glucose oxidation.
- Decreased protein iodination and intracellular myeloperoxidase were observed in affected PMNs.
- A significant bactericidal defect was identified, while phagocytosis remained normal.
Conclusions:
- Canine cyclic neutropenia is characterized by significant PMN metabolic and functional abnormalities.
- These PMN defects are distinct from chronic granulomatous disease and Chediak-Higashi syndrome.
- The findings suggest a resemblance to hereditary myeloperoxidase deficiency, highlighting defective PMN function.