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Correction of canine cyclic hematopoiesis with recombinant human granulocyte colony-stimulating factor
C D Lothrop1, D J Warren, L M Souza
1Department of Environmental Practice, College of Veterinary Medicine, University of Tennessee, Knoxville 37901.
Insights
Canine cyclic hematopoiesis (CH) is a neutrophil disorder in dogs. Recombinant human granulocyte colony-stimulating factor (rhG-CSF) temporarily corrected neutrophil levels and prevented neutropenic episodes in CH dogs.
Area of Science:
- Hematology
- Veterinary Medicine
- Genetics
Background:
- Canine cyclic hematopoiesis (CH) is an inherited disorder in gray collies.
- CH involves periodic neutropenic episodes due to an unknown regulatory defect.
- This condition affects neutrophil production and regulation.
Purpose of the Study:
- To investigate the efficacy of recombinant human granulocyte colony-stimulating factor (rhG-CSF) in managing canine cyclic hematopoiesis.
- To assess the impact of rhG-CSF on neutrophil counts and progenitor cell dynamics in CH dogs.
- To explore rhG-CSF as a potential therapeutic agent for cyclic neutropenia.
Main Methods:
- Administration of rhG-CSF to two CH dogs and one normal dog.
- Monitoring of white blood cell (WBC) counts, including neutrophils and monocytes.
- Bone marrow evaluation to assess myeloid/erythroid progenitor cell populations.
Main Results:
- rhG-CSF induced marked leukocytosis (primarily neutrophils) in all dogs.
- Neutropenic episodes were prevented in CH dogs during rhG-CSF treatment.
- Bone marrow progenitor cell fluctuations characteristic of CH were normalized.
- Antibody development against rhG-CSF led to a decline in WBC counts.
Conclusions:
- rhG-CSF can temporarily alleviate the regulatory defect in canine cyclic hematopoiesis.
- The study suggests rhG-CSF as a potential treatment for canine CH.
- Findings indicate potential applicability for treating human cyclic neutropenia.
Abstract:
Canine cyclic hematopoiesis (CH) is an autosomal recessive disease of gray collie dogs that is characterized by neutropenic episodes at 14-day intervals. The biochemical basis for CH is not known but may involve a regulatory defect of the response to or production of a hematopoietic growth factor. Administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) to two CH and one normal dog caused a marked leukocytosis (greater than 50,000 WBCs) in all three dogs. The leukocytosis was due largely to a greater than tenfold increase in neutrophils. Less pronounced but significant elevations in monocytes occurred during G-CSF treatment. The elevated WBC count was maintained for more than 20 days in all three dogs, and two predicted neutropenic episodes were prevented in both CH dogs during rhG-CSF treatment. A decline in the WBC count occurred simultaneously in all three dogs during the last five treatment days and was presumably associated with the development of neutralizing antibodies to the heterologous rhG-CSF protein. Bone marrow evaluation indicated that the swings in the myeloid/erythroid progenitor cells that are characteristic of CH were eliminated by rhG-CSF treatment in both CH dogs. These results suggest that the regulatory defect in canine CH can be temporarily alleviated by treatment with rhG-CSF and point to the potential treatment of human cyclic neutropenia with this agent.