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Effect of lung surfactant on the release of factor increasing monocytopoiesis by macrophages
W Sluiter1, L W van Hemsbergen-Oomens, I Elzenga-Claasen
1Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
Abstract:
Upon ingestion of particulate and soluble material, at the site of an inflammation macrophages release the factor increasing monocytopoiesis (FIM), which accelerates the rate of division of the monoblasts and promonocytes in the bone marrow. It is not known, however, whether FIM is released by macrophages present at noninflamed sites. Since FIM is secreted only during phagocytosis and alveolar macrophages ingest surfactant in vivo, the present study was performed to find out whether surfactant induces the release of FIM by alveolar macrophages. Resident alveolar macrophages were found to contain FIM and secrete this factor in vitro in the absence of an introduced phagocytable particle. Resident peritoneal macrophages also contained FIM and released this factor after exposure to surfactant. These findings suggest that in the absence of an inflammatory stimulus in vivo, alveolar macrophages that have ingested surfactant release FIM to maintain the normal production of monocytes in the bone marrow.
Insights
Macrophages release a factor increasing monocytopoiesis (FIM) during inflammation. This study shows surfactant exposure causes macrophages to release FIM, maintaining normal monocyte production without inflammation.
Area of Science:
- Immunology
- Hematopoiesis
- Cell Biology
Background:
- Macrophages are key immune cells involved in inflammation.
- During inflammation, macrophages release a factor increasing monocytopoiesis (FIM).
- It remains unclear if macrophages at non-inflamed sites release FIM.
Purpose of the Study:
- To investigate if surfactant exposure induces FIM release by alveolar macrophages.
- To determine if FIM is released by macrophages in the absence of inflammatory stimuli.
Main Methods:
- Resident alveolar macrophages were cultured in vitro.
- Resident peritoneal macrophages were exposed to surfactant.
- FIM secretion was measured in both conditions.
Main Results:
- Resident alveolar macrophages contained and secreted FIM in vitro without added particles.
- Resident peritoneal macrophages released FIM after exposure to surfactant.
- These findings indicate FIM release can occur independently of overt inflammation.
Conclusions:
- Surfactant ingestion by alveolar macrophages can trigger FIM release.
- This mechanism may maintain normal monocyte production in non-inflammatory conditions.
- Macrophages play a role in regulating hematopoiesis even in the absence of inflammation.