Loss of Fcγ receptor and impaired phagocytosis of polymorphonuclear leukocytes in gingival crevicular fluid

Immunoglobulin G type II and III receptors (FcγRII and FcγRIII) are essential for polymorphonuclear leukocytic (PMNs) phagocytosis. Our previous study demonstrated a downregulation of FcγRIII on PMNs in gingival crevicular fluid (GCF). To determine whether this receptor downregulation may contribute to the periodontal host defence borne by PMNs, we examined the correlation between FcγRII and FcγRIII expressions and the phagocytic capacity of GCF‐PMNs. In order to verify at which level of cellular events the loss of FcγR occurs, we quantified mRNA levels to assess a de novo synthesis of these receptors. GCF was collected from 21 patients with adult periodontitis by gingival crevicular washing. Autologous peripheral blood (PB) PMNs served as control. Surface expressions of FcγRs and phagocytic capacity via FcγRs were analysed by flow cytometry. The difference in FcγR mRNA levels between GCF‐ and PB‐PMNs was assessed by reverse transcription‐polymerase chain reaction (RT‐PCR). The amplified products were visualized by agarose gel electrophoresis and the endproduct yields were quantified by computerized image‐analysis. Both FcγRII and FcγRIII expressions and phagocytic capacity on GCF‐PMNs were significantly lower than those on PB‐PMNs (p < 0.001). The downregulation of FcγRs on GCF‐PMNs significantly correlated with the phagocytic capacity (r = 0.66 for FcγRIII, p < 0.01; r = 0.50 for FcγRII, p < 0.05). The mRNA level of FcγRIII of GCF‐PMNs was significantly lower than that of PB‐PMNs (p < 0.05). Thus, GCF‐PMNs are characterized by the decreased surface expressions and mRNA levels of FcγRs, and the impaired phagocytosis.