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Pulmonary macrophage function in systemic gadolinium chloride-pretreated rats
G Bannenberg1, M Lundborg, A Johansson
1Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Toxicology Letters
|October 1, 1995
Summary
Systemic gadolinium chloride pretreatment did not inhibit rat pulmonary macrophage function. Even at higher doses, neither phagocytosis nor nitroblue tetrazolium reduction by alveolar and interstitial macrophages was affected.
Area of Science:
- Immunology
- Toxicology
- Respiratory Medicine
Background:
- Pulmonary macrophages are crucial for lung immunity.
- Gadolinium chloride is known to inhibit Kupffer cells (liver macrophages).
- The effect of gadolinium chloride on pulmonary macrophages is not well-established.
Purpose of the Study:
- To investigate the efficacy of systemic gadolinium chloride pretreatment in inhibiting rat pulmonary macrophage function.
- To determine if gadolinium chloride affects phagocytosis and nitroblue tetrazolium reduction in alveolar and interstitial macrophages.
Main Methods:
- Rats were pretreated with gadolinium chloride (10 mg/kg or 20 mg/kg) intravenously 48 hours before sacrifice.
- Alveolar and interstitial macrophages were isolated.
- Phagocytosis and nitroblue tetrazolium reduction assays were performed.
Main Results:
- Gadolinium chloride administration at 10 mg/kg and 20 mg/kg showed no significant effect on pulmonary macrophage phagocytosis.
- Nitroblue tetrazolium reduction by pulmonary macrophages remained unaffected by gadolinium chloride pretreatment.
- These results indicate a lack of inhibitory effect on pulmonary macrophages at doses effective for Kupffer cell inhibition.
Conclusions:
- Systemic gadolinium chloride pretreatment does not inhibit the function of rat alveolar and interstitial macrophages.
- The dose and timing of administration that inhibit Kupffer cells do not translate to pulmonary macrophages.
- Gadolinium chloride is not a suitable agent for modulating pulmonary macrophage activity in vivo.