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Factors affecting SP-A-mediated phagocytosis in human monocytic cell lines
Jianqiang Ding1, Todd M Umstead, Joanna Floros
1Department of Cellular Physiology, Pennsylvania State College of Medicine, P.O. Box 850, Hershey, PA 17033, USA.
Abstract:
Surfactant protein-A enhances the phagocytosis and killing of many pathogens, although studying this effect in an assortment of models and different experimental protocols has sometimes yielded conflicting results. In this report, using the human THP-1 cell line as the primary phagocytic cell, we systematically examined several models where microspheres, Staphylococcus aureus and Escherichia coli were used for targets. We found that SP-A derived from human lavage appeared to enhance phagocytosis by two different mechanisms; by SP-A binding of the target to enhance its recognition and subsequent phagocytosis and by a direct SP-A stimulatory effect on the phagocyte itself. Both SP-A mechanisms occurred with different targets in the same experimental system and the SP-A effects were qualitatively (but not quantitatively) comparable in several human cell lines (THP-1, U937, Mono-Mac-6). We also found that the SP-A effects were abrogated when SP-A was combined with surfactant lipids, but the lipids did not affect the basal level of phagocytosis or phagocytosis by mechanisms not involving SP-A. Moreover, the stimulatory effect of SP-A was pH-dependent and appeared to be independent of several other phagocytic mechanisms, including those mediated by Fc receptors and mannose receptor.
Insights
Surfactant protein-A (SP-A) enhances pathogen clearance by immune cells through direct binding and by stimulating phagocytes. These SP-A effects are pH-dependent and influenced by surfactant lipids.
Area of Science:
- Immunology
- Biochemistry
- Cell Biology
Background:
- Surfactant protein-A (SP-A) is known to enhance phagocytosis and pathogen killing.
- Previous studies have reported conflicting results regarding SP-A's efficacy due to varied experimental models and protocols.
Purpose of the Study:
- To systematically investigate the mechanisms by which SP-A enhances phagocytosis using human THP-1 cells and various targets.
- To elucidate the influence of surfactant lipids and pH on SP-A-mediated phagocytosis.
Main Methods:
- Utilized human THP-1 cell line as the primary phagocytic model.
- Employed microspheres, Staphylococcus aureus, and Escherichia coli as targets.
- Assessed SP-A's effects on phagocytosis, including mechanisms involving target binding and direct phagocyte stimulation.
- Investigated the impact of surfactant lipids and pH on SP-A activity.
Main Results:
- SP-A enhanced phagocytosis via two distinct mechanisms: target recognition/binding and direct stimulation of phagocytes.
- These SP-A effects were observed with different targets and were qualitatively similar across THP-1, U937, and Mono-Mac-6 cell lines.
- SP-A's stimulatory effects were abrogated by surfactant lipids but not by Fc receptor or mannose receptor pathways.
- The SP-A stimulatory effect was found to be pH-dependent.
Conclusions:
- SP-A plays a significant role in innate immunity by enhancing phagocytosis through multiple mechanisms.
- Understanding these mechanisms, including their modulation by lipids and pH, is crucial for harnessing SP-A's therapeutic potential.
- SP-A's distinct pathways offer insights into targeted immune modulation strategies.
