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A functional comparison of blood and gingival inflammatory polymorphonuclear leucocytes in man
Abstract:
Polymorphonuclear leucocytes from the human gingival crevice (CREV-PMN) have a defective phagocytic capacity when compared with peripheral blood polymorphonuclear leucocytes (PB-PMN) from the same individual. In a study of fourteen clinically healthy subjects, significantly smaller numbers of CREV-PMN phagocytosed fewer Candida albicans blastospores as compared with PB-PMN. The intracellularkilling capacity of the two cell populations was similar. Removal of specific antibody but not complement significantly depressed blastospore uptake by both cell types. It is postulated that the intrinsic defect of the CREV-PMN is acquired in vivo and may be a general property of PMN from inflammatory sites.
Insights
Human gingival crevice neutrophils (CREV-PMN) show reduced phagocytosis of Candida albicans compared to peripheral blood neutrophils (PB-PMN). This defect, potentially acquired in vivo, impacts immune response at inflammatory sites.
Area of Science:
- Immunology
- Oral Microbiology
- Cell Biology
Background:
- Polymorphonuclear leucocytes (PMNs) are crucial immune cells.
- Neutrophils from the gingival crevice (CREV-PMN) may exhibit altered function compared to peripheral blood neutrophils (PB-PMN).
Purpose of the Study:
- To compare the phagocytic capacity of CREV-PMN and PB-PMN.
- To investigate the role of antibody and complement in CREV-PMN phagocytosis.
Main Methods:
- Phagocytosis assays using Candida albicans blastospores.
- Comparison of CREV-PMN and PB-PMN from fourteen healthy subjects.
- Assessment of the effect of antibody and complement removal on phagocytosis.
Main Results:
- CREV-PMN demonstrated significantly lower phagocytosis of Candida albicans blastospores than PB-PMN.
- Intracellular killing capacity was similar between CREV-PMN and PB-PMN.
- Removal of specific antibody, but not complement, reduced blastospore uptake in both cell types.
Conclusions:
- Gingival crevice neutrophils possess an intrinsic defect in phagocytic capacity.
- This defect is likely acquired in vivo and may be characteristic of neutrophils from inflammatory sites.
- Specific antibodies play a significant role in neutrophil-mediated fungal clearance.