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Bioavailability of granulocyte colony-stimulating factor administered enterally to suckling mice
Jason A Gersting1, Catherine A Kotto-Kome, Yan Du
1Department of Pediatrics, Division of Neonatology, University of Florida, Gainesville, FL 32610-0296, USA.
Insights
Granulocyte colony-stimulating factor (G-CSF) shows minimal absorption (<1%) into the circulation after enteral administration in suckling mice. The granulocyte CSF receptor (G-CSF-R) is not essential for this limited absorption process.
Area of Science:
- Developmental Biology
- Gastroenterology
- Hematology
Background:
- The developing gastrointestinal (GI) tract is influenced by various growth factors.
- Granulocyte colony-stimulating factor (G-CSF) is present in high concentrations in fetal and neonatal nutrition sources.
- G-CSF receptors (G-CSF-R) are expressed on intestinal enterocytes, suggesting a potential role in GI development.
Purpose of the Study:
- To investigate the systemic absorption of enterally administered recombinant human G-CSF (rhG-CSF) in suckling mice.
- To determine if the G-CSF receptor (G-CSF-R) is necessary for the absorption of orally administered G-CSF.
Main Methods:
- Enteral administration of rhG-CSF to suckling mice at doses of 3 ng or 300 ng.
- Testing pups at 5-7 days and 14-16 days of age.
- Utilizing mice with and without a functional G-CSF-R gene.
Main Results:
- The bioavailability of enterally administered G-CSF was consistently less than 1%.
- Absorption was minimal regardless of G-CSF dose, pup age, or G-CSF-R functionality.
- G-CSF receptor status did not influence the low absorption rates observed.
Conclusions:
- Enteral G-CSF administration results in negligible systemic absorption in suckling mice.
- The G-CSF receptor is not a critical factor for the limited absorption of G-CSF from the gut.
Abstract:
The developing fetal and neonatal gastrointestinal (GI) tract is influenced by many growth factors, including epidermal growth factor (EGF), insulin-like growth factor (IGF), transforming growth factor (TGF), and erythropoietin (Epo). Granulocyte colony-stimulating factor (G-CSF), typically regarded as a hematopoietic growth factor, might also be included because it exists in high concentrations in amniotic fluid, colostrum, and human milk, and because granulocyte CSF receptors (G-CSF-R) are abundantly expressed on the villous enterocytes of the developing intestine. As a first step toward understanding whether the effects of G-CSF on the GI tract were local or systemic, we sought to determine whether recombinant human G-CSF (rhG-CSF) administered enterally to suckling mice, is absorbed into the circulation, and if so, whether the G-CSF-R is essential for this absorption. We enterally administered rhG-CSF to suckling mice, selecting a daily dose based on the amount of G-CSF normally swallowed by the fetus and neonate (3 ng), or in other mice, a dose of G-CSF 100 times larger (300 ng). Pups were tested at either 5-7 days of age, or at 14-16 days of age. C57BL/6 x 129SvJ mice were used. Some mice had a targeted null mutation in the G-CSF-R gene, producing a non-functional G-CSF-R protein. At intervals following the enteral G-CSF dosing, G-CSF concentrations in plasma were measured by specific ELISA. The bioavailability of G-CSF was invariably <1%, regardless of the dose of rhG-CSF given, the age of the pups, or whether they had a functional G-CSF-R. After enteral administration of rhG-CSF to suckling mice, only minimal quantities of G-CSF are absorbed into the circulation, and the G-CSF-R is not essential for this absorption.
