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Variance in expression of receptors for immunoglobulin G (FcγRs), complement (CR3) and lipopolysaccharide (mCD14) on polymorphonuclear neutrophils (PMNs) and monocytes might affect susceptibility for infection with certain pathogens in periodontitis, a chronic infectious disease of tooth-supportive tissues. Levels of FcγRI, IIa, III, CR3 and mCD14 on PMNs and monocytes were measured in 19 periodontitis patients and 18 healthy controls. Subgingival infection with Aggregatibacter actinomycetemcomitans ( Aa) and Porphyromonas gingivalis ( Pg) was determined. Activation of PMNs and monocytes in response to stimulation with Aa and Pg was assessed by means of change in mCD14 expression. Periodontitis is associated with an enrichment of the FcγRIII+ monocytes ( P = 0·015) with concomitant low mCD14 ( P = 0·001). Unadjusted data showed that the subjects culture-positive for Aa ( Aa+) had significantly lower expression of monocytic FcγRI ( P = 0·005) and FcγRIIa ( P = 0·015) than Pg+ subjects. The FcγRI was still lower on monocytes from Aa+ subjects after adjusting for the background factors ( P = 0·037). PMNs from Aa+ subjects responded in a hyper-reactive manner, in particular when stimulated with Aa ( P = 0·011). Lower FcγRs expression by monocytes is related to a higher susceptibility of a subject to become infected with Aa. The higher proportion of FcγRIII+ monocytes may be involved in the chronicity of this condition. Hyper-reactive PMNs in Aa+ subjects may contribute to accelerated breakdown of tooth-supportive tissues. [ABSTRACT FROM AUTHOR]

Summary Bacteria colonizing tooth surfaces are essential in the induction of an inflammatory response in the periodontal tissues, but do not cause periodontitis in everyone, implicating differences in the host immune response. These possible differences were studied using lipopolysaccharide (LPS)-stimulated whole blood cell cultures (WBCC), which revealed a down regulation of monocyte derived interleukin-12 (IL-12p70) in untreated periodontitis patients and an up regulation after therapy. IL-12p70 is a crucial factor in the differentiation of Th1 cell responses. Since CC chemokines are able to influence the T cell differentiation via cytokine secretion in antigen-presenting cells, the production of CC chemokines in periodontitis was evaluated. Therefore WBCC were stimulated with LPS from Escherichia coli for 18 h and the levels of IL-12p70 and CC chemokines were measured in the supernatants by ELISA. Untreated periodontitis patients released 2 fold more RANTES (regulated on activation normal T cell expressed and secreted) (P = 0·01) and lower levels of IL-12p70 in comparison to controls (P < 0·05). A trend towards higher levels of macrophage chemoattractant protein-1 (MCP-1) (P = 0·07) was also seen in untreated periodontitis patients; while similar levels of monocyte derived chemokine (MDC) and macrophage inflammatory proteins-1α and -1β (MIP-1α and -1β ) were found. After periodontal therapy no changes were seen with regard to MDC, MIP-1α , MIP-1β and RANTES, whereas the MCP-1 levels decreased (P < 0·05) and the IL-12p70 levels strongly increased (P < 0·01). The data showed a consistent inverse correlation between the levels of MCP-1 and IL-12p70, and their proportional changes after therapy correlated with the clinical inflammatory response after therapy. This indicates that the disease state regulates the release of IL-12p70 and MCP-1 in E. coli LPS-stimulated WBCC. In contrast, the persistent... [ABSTRACT FROM AUTHOR]

SUMMARY It is acknowledged that periodontitis results from the interaction of the host immune response with bacteria accumulating on the tooth surfaces. Although bacteria are essential, they are insufficient to cause the disease. Despite this knowledge it remains unclear why certain individuals are more susceptible to periodontitis than others. Therefore the present study investigated whether differences exist in the actual immune response between periodontitis patients and controls after stimulation of peripheral blood cells. Whole blood cell cultures (WBCC) were stimulated with LPS from Escherichia coli during 18 h and the release of prostaglandin E2 (PGE2 ), IL-1β, IL-6, IL-8, IL-10, IL-12p40, IL-12p70 and tumour necrosis factor-alpha (TNF-α) was measured. The levels of PGE2 were two-fold higher in the WBCC from periodontitis patients than from controls. In contrast, the levels of IL-12p70 in WBCC from patients were two-fold lower. Furthermore, WBCC from patients secreted lower levels of IL-1β and higher levels of IL-8 when compared with WBCC from controls. No differences were observed with respect to IL-6, IL-10, IL-12p40 and TNF-α production. It is known from the literature that LPS-stimulated WBCC reflect specifically the behaviour of the monocytes and that monocytes are peripheral precursors of antigen-presenting cells (APC). Therefore it is concluded that the monocytes in the present WBCC from periodontitis patients are responsible for the higher levels of PGE2 and lower levels of IL-12p70. Since it is has been shown that APC-derived IL-12p70 induces type (Th1) cells that promote cellular immunity, while APC-derived PGE2 induces type 2-helper (Th2) cells that promote humoral immunity, it is postulated that APC from periodontitis patients may have a bias in directing Th2 responses and thereby promoting the humoral immunity in periodontitis. [ABSTRACT FROM AUTHOR]