Interaction of Fusobacterium nucleatum 191 with human peripheral blood lymphocytes

Abstract

Fusobacterium nucleatum is frequently isolated in high numbers from the subgingival plaque of patients with periodontal diseases. Adherence of these bacteria to several host tissues is lectin-like in that it is inhibited by galactose, lactose, and N-acetyl-galactosamine. Since F. nucleatum has the capacity to activate human peripheral blood lymphocytes, the purpose of this study was to determine whether F. nucleatum adheres to lymphocytes and, if so, to determine whether lectin-like interactions facilitate lymphocyte activation. Adherence of F. nucleatum strain 191 to lymphocytes was confirmed by agglutination assays, scanning electron microscopy, and by using fluorescein- or [3H]-labeled bacteria. Saturation of adherence was reached at about 35 bacteria per lymphocyte. F. nucleatum adhered to greater than 90% of the lymphocytes, and adhered in higher numbers to B cell-enriched subpopulations than to T cell-enriched subpopulations. Adherence was inhibited by N-acetyl-galactosamine, lactose greater than galactose, alpha- and beta-methyl galactoside, but not by 100 mM glucose, mannose, N-acetyl-glucosamine, or other sugars tested. Lymphocytes underwent mitogenesis when preincubated with bacteria and washed to remove weakly adherent and non-adherent bacteria. Mitogenesis induced by low concentrations of F. nucleatum was reduced, but not completely eliminated, by N-acetyl-galactosamine. However, N-acetyl-galactosamine had no effect on mitogenesis induced by preincubation with high concentrations of bacteria. These results suggest that adherence of F. nucleatum facilitates activation of lymphocytes, particularly at low concentrations of bacteria.

Effect of sonicated material from Fusobacterium nucleatum on the functional capacity of accessory cells derived from dental pulp

“…Second, when pulpal accessory cells were pretreated with the bacterial components, the subsequent proliferation of T-lymphocytes increased significantly. These findings may be explained by an adherence of components from F. nucleatwn to the cell membrane of the accessory cells as the first step (24). As the second step, signals necessary to initiate an increased proliferative response of the Tlymphocytes may have been induced by the bacterial components.…”

Fusobacterium nucleatum Transports Noninvasive Streptococcus cristatus into Human Epithelial Cells

“…Additionally, F. nucleatum adheres to erythrocytes (6,12,48), polymorphonuclear leukocytes (20,30,37), and lymphocytes (57,58,64). It also binds fibronectin (1) and plasminogen (5).…”

Lipid peroxidation caused by oxygen radicals from Fusobacterium‐stimulated neutrophils as a possible model for the emergence of periodontitis

“…The disease may progress for many years without significant discomfort for the patient (Heimdahl and Nord, 1985). The microbial flora associated with subgingival plaques in humans with periodontal disease is believed to cause an inflammatory response and destruction of the gingival tissues (Passo et al , 1982; Tuttle and Mangan, 1990; Edlund et al , 1996). This flora consists mainly of Porphyromonas gingivalis (Fenesy, 1998) but also of other anaerobic cocci, Bacteroides sp, Fusobacterium sp, Capnocytophaga sp, Selenomonas sp, and Treponema sp.…”

“…(Passo et al , 1982; Heimdahl and Nord, 1985). Fusobacterium species are Gram‐ negative anaerobic bacteria (Tuttle and Mangan, 1990; Ding et al , 1997), and are common in almost all dental plaque samples, since they have a great capacity to coaggregate with all other oral bacteria (Darveau et al , 1997). Fusobacterium nucleatum , often present in chronic adult periodontitis (Seow and Thong, 1986; Tuttle et al , 1992), is also a strong inducer of lymphocyte mitogenesis and polyclonal immunoglobulin production and may be important in nonspecific activation of cells in periodontal lesions (Tuttle et al , 1992).…”