Human plasmacytoid dendritic cells (PDC) are key sentinels alerting both innate and adaptive immune responses through production of huge amounts of alpha/beta interferon (IFN). IFN induction in PDC isSuccessful defense against invading pathogens involves rapid recognition of conserved danger signals through members of the Toll-like receptor (TLR) protein family (1) and induction of cytokines that activate both innate and adaptive immunity. A principal effector integrating early antiviral and immunostimulatory activities is the alpha/beta interferon (IFN) system, including the group of IFN-␣ isotypes and IFN-␤ (21). Although most types of cells can produce IFN through recognition of cytosolic double-stranded RNA (1a, 36, 44), or upon stimulation of TLR3 and TLR4 through double-stranded RNA or lipopolysaccharide, respectively (1), the vast amount of IFN upon entry of bacterial and viral pathogens is produced by a specialized cell population, plasmacytoid dendritic cells (PDC) (2, 6). Transcriptional induction of IFN genes is controlled by interferon regulatory factors (IRFs). IRF-3 mainly regulates IFN-␤ induction, whereas IRF-7 has the ability to activate IFN-␣ promoters (22,25,45). In contrast to other cell types, PDC constitutively express high levels of IRF-7 such that expression of IFN-␣ by PDC is independent of the IFN-␣ receptor-mediated positive feedback via IFN-␤ (3, 13, 16, 18), explaining in part the promptness of high-capacity IFN-␣ production.The TLR repertoire of human PDC is composed of TLR7 and TLR9, both located in the endosomal membrane. As shown recently, TLR7 and TLR8 recognize viral singlestranded RNA (8, 12) as well as imidazoquinolines such as imiquimod and resiquimod (R848) and guanosine analogs (reviewed in references 1 and 42). In contrast, TLR9 recognizes bacterial or viral DNA (1), including synthetic CpG oligodeoxynucleotides (ODN) (11). Indeed, recent work revealed IFN-␣ production in PDC after incubation with a variety of inactivated or live DNA and RNA viruses, including herpes simplex virus types 1 and 2 (16,19,23), murine cytomegalovirus (7), human immunodeficiency virus (46), influenza A virus (8,24), Sendai virus (14,16), and vesicular stomatitis virus (3,24). For herpes simplex virus (19,23), Influenza A virus (8,24), and vesicular stomatitis virus (24), the critical involvement of MyD88 adaptor-dependent TLR9 and TLR7 signaling has been demonstrated.In addition to perceiving external virus components through TLR7 and TLR9, human PDC have the means to sense cytosolic replicating RNA viruses. As we could show recently, respiratory syncytial virus (RSV) escapes from recognition by PDC TLRs (14). Nevertheless, infection with a particular laboratory strain of RSV (subtype A, strain Long), or cytosolic delivery of double-stranded RNA but not of poly(I:C) led to potent IFN-␣ induction in PDC in a TLR-and protein kinase R-independent manner (14).The considerable repertoire of tools for sensing pathogens combined with a tremendous capacity to produce IFN make human PDC the key sentinel...

Periodontal disease involves complex interactions of microorganisms and host defenses. This work investigated the associations between putative bacterial pathogens, herpesviruses and chronic periodontitis. Subgingival samples were collected from 40 periodontally healthy individuals and from 40 patients with chronic periodontitis with probing depths of < or =3 mm or > or =6 mm. Multiplex and nested polymerase chain reactions were used to identify bacterial pathogens and herpesviruses. Porphyromonas gingivalis, Tannerella forsythia, Epstein-Barr virus (EBV) type 1, cytomegalovirus (CMV), Aggregatibacter actinomycetemcomitans and EBV type 2 were detected in, respectively, 95, 75, 72.5, 50, 12.5 and 10% of sites with probing depths > or =6 mm. P. gingivalis, T. forsythia, EBV-1 and CMV were statistically associated with probing depths > or =6 mm. A. actinomycetemcomitans and EBV-2 showed no association with periodontitis sites, and no significant associations were found for any of the test infectious agents and probing depths < or =3 mm. Our results confirm an association between P. gingivalis, T. forsythia, EBV-1 and CMV, and chronic periodontitis. These infectious agents may play an important synergistic role in the pathogenesis of chronic periodontitis.

Background:Helicobacter pylori (H. pylori) is a spiral Gram negative bacteria that can transform to the coccoid form in adverse conditions.Objectives:The aim of this study was to determine the in vitro morphological and bactericidal effects of metronidazole, amoxicillin and clarithromycin on H. pylori.Materials and Methods:The standard strain 26695 of H. pylori was cultured on Brucella agar (BA) and the minimum inhibitory concentrations (MICs) of three antibiotics were determined by E-test method. The bacteria were exposed to antibiotics at 1/2 MIC, MIC and 2X MIC concentrations in Brucella broth (BB). Induced coccoid forms were confirmed by Gram staining and light microscopy. The viability of cells as well as the susceptibility of viable coccoids to antibiotics were examined using the flow cytometry method.Results:All of the three antibiotics at sub-MIC induced coccoid forms. The highest rates of coccoids (> 90%) were induced at 0.008 μg/mL concentration (1/2 MIC) of amoxicillin, 72 hours postexposure. Metronidazole and clarithromycin with 1/2 MIC (0.5 and 0.125 µg/mL respectively) induced lower rates of coccoid forms (60% and 40% respectively). Potent bactericidal effects on coccoids were observed with Metronidazole at 2X MIC and clarithromycin at MIC (0.25 µg/mL) (80 - 90%). Amoxicillin with MIC and 2X MIC had no bactericidal effect on coccoid forms.Conclusions:Despite the good in vitro bactericidal effect of amoxicillin on spiral forms of H. pylori, this antibiotic has little effect on induced coccoids that may develop after the inappropriate in vivo antibacterial treatment. Hence, for successful therapy, it is essential not only to eradicate the spiral forms, but to eliminate the viable coccoids.

Periodontitis is an infectious disease involving specific bacteria and viruses. Herpesviruses believed to play roles in it. The present study examines the presence of Epstein-Barr virus (EBV) and cytomegalovirus (CMV) in subgingival and supragingival plaque of 61 patients with chronic periodontitis and 40 healthy controls. A nested polymerase chain reaction method was used. The clinical parameters, clinical attachment level (CAL), probing depth (PD) and bleeding on probing (BOP) were examined. Prevalence of EBV- 1, EBV-2 and CMV were 73.8%, 4.9% and 59%; respectively. There was no association between the presence of EBV-1, EBV-2 and CMV with bleeding on depth.

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