General immune status and oral microbiology in patients with different forms of periodontitis and healthy control subjects.

OBJECTIVE: Immunological processes in the etiopathogenesis of periodontitis, especially the aggressive form, are not well understood. This study examined clinical as well as systemic immunological and local microbiological features in healthy controls and patients with different forms of periodontitis. MATERIALS AND METHODS: 14 healthy subjects, 15 patients diagnosed with aggressive periodontitis, and 11 patients with chronic periodontitis were recruited. Periodontal examination was performed and peripheral blood was collected from each patient. Lymphocyte populations as well as the release of cytokines by T-helper cells were determined by flow cytometry and enzyme linked immunosorbent spot assay. Subgingival plaque samples were taken from each individual and immediately cultivated for microbiological examination. RESULTS: When stimulating peripheral blood mononuclear cells (PBMCs) with lipopolysaccharide, a higher IL-1ß release was found in patients with moderate chronic periodontitis compared to the other groups (p<0.01). Numbers of B-cells, naïve and transitional B-cells, memory B-cells, and switched memory B-cells were within the reference range for all groups, but patients with chronic periodontitis showed the highest percentage of memory B-cells without class switch (p = 0.01). The subgingival plaque differed quantitatively as well as qualitatively with a higher number of Gram-negative anaerobic species in periodontitis patients. Prevotella denticola was found more often in patients with aggressive periodontitis (p<0.001) but did not show an association to any of the systemic immunological findings. Porphyromonas gingivalis, which was only found in patients with moderate chronic periodontitis, seems to be associated with an activation of the systemic immune response. CONCLUSION: Differences between aggressive periodontitis and moderate chronic periodontitis are evident, which raises the question of an inadequate balance between systemic immune response and bacterial infection in aggressive periodontitis.

IgM production by bone marrow plasmablasts contributes to long-term protection against intracellular bacterial infection.

IgM responses are well known to occur early postinfection and tend to be short-lived, which has suggested that this Ig does not significantly contribute to long-term immunity. In this study, we demonstrate that chronic infection with the intracellular bacterium Ehrlichia muris elicits a protective, long-term IgM response. Moreover, we identified a population of CD138(high)IgM(high) B cells responsible for Ag-specific IgM production in the bone marrow. The IgM-secreting cells, which exhibited characteristics of both plasmablasts and plasma cells, contributed to protection against fatal ehrlichial challenge. Mice deficient in activation-induced cytidine deaminase, which produce only IgM, were protected against fatal ehrlichial challenge infection. The IgM-secreting cells that we have identified were maintained in the bone marrow in the absence of chronic infection, as antibiotic-treated mice remained protected against challenge infection. Our studies identify a cell population that is responsible for the IgM production in the bone marrow, and they highlight a novel role for IgM in the maintenance of long-term immunity during intracellular bacterial infection.

B cell precursors are targets for Salmonella infection.

We previously reported that, in mice, B cells are a reservoir for bacteria during Salmonella infection. Here, we show that, within the bone marrow, B cells and their precursors are targeted for infection by Salmonella enterica serovar typhimurium. Our data suggest that B cells within the bone marrow may be a bacterial niche during chronic Salmonella infection.