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J Periodontal Res. 2003 Jun;38(3):318-23.
The herpesvirus-Porphyromonas gingivalis-periodontitis axis.

Slots J, Kamma JJ, Sugar C.

University of Southern California, School of Dentistry, Los Angeles, CA 90089-0641, USA. jslotsc.edu

OBJECTIVES AND BACKGROUND: Members of the herpesvirus family have accumulated considerable support for a role in severe types of periodontitis. This study aimed to examine whether human cytomegalovirus (HCMV), Epstein-Barr virus type 1 (EBV-1) or herpes simplex virus (HSV) together with the major periodontopathic bacterium Porphyromonas gingivalis might interact in the pathogenesis of periodontal breakdown. METHODS: Sixteen subjects each contributed paper point samples from two progressing and two stable periodontitis lesions, as determined by ongoing loss of probing attachment. Polymerase chain reaction methodology was used to identify subgingival herpesviruses, P. gingivalis and other bacterial pathogens. Chi-squared tests and multivariate logistic regression were employed to identify statistical associations between herpesviruses, periodontopathic bacteria and clinical variables. RESULTS: HCMV and HSV were both significant predictors of the presence of subgingival P. gingivalis. In turn, P. gingivalis was positively associated with periodontitis active disease, probing attachment level, probing pocket depth, gingival bleeding upon probing and patient age. EBV-1 was not linked to P. gingivalis, although the virus was predictive of periodontitis active disease. The periodontitis disease risk associated with herpesvirus-P. gingivalis combinations depended on both site-specific and subject-specific factors. CONCLUSION: The present data of aggressive periodontitis implicate HCMV, HSV and P. gingivalis as either cofactors in its etiology or triggers of relapses. Further studies are needed to determine the spectrum of periodontopathogenicity of herpesviruses and effective management of these viruses in periodontal sites.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12753371&dopt=Abstract

Pigment Cell Res. 2003 Jun;16(3):208-14.
Epidemiology of vitiligo and associated autoimmune diseases in caucasian probands and their families.

Alkhateeb A, Fain PR, Thody A, Bennett DC, Spritz RA.

Human Medical Genetics Program, University of Colorado Health Sciences Center, Denver, CO, USA. richard.spritchsc.edu

Generalized vitiligo is an autoimmune disorder characterized by acquired white patches of skin and overlying hair, the result of loss of melanocytes from involved areas. The most common disorder of pigmentation, vitiligo occurs with a frequency of 0.1-2.0% in various populations. Family clustering of cases is not uncommon, in a non-Mendelian pattern suggestive of multifactorial, polygenic inheritance. We surveyed 2624 vitiligo probands from North America and the UK regarding clinical characteristics, familial involvement, and association with other autoimmune disorders, the largest such survey ever performed. More than 83% of probands were Caucasians, and the frequency of vitiligo appeared approximately equal in males and females. The frequency of vitiligo in probands' siblings was 6.1%, about 18 times the population frequency, suggesting a major genetic component in disease pathogenesis. Nevertheless, the concordance of vitiligo in monozygotic twins was only 23%, indicating that a non-genetic component also plays an important role. Probands with earlier disease onset tended to have more relatives affected with vitiligo, suggesting a greater genetic component in early onset families. The frequencies of six autoimmune disorders were significantly elevated in vitiligo probands and their first-degree relatives: vitiligo itself, autoimmune thyroid disease (particularly hypothyroidism), pernicious anaemia, Addison's disease, systemic lupus erythematosus, and probably inflammatory bowel disease. These associations indicate that vitiligo shares common genetic aetiologic links with these other autoimmune disorders. These results suggest that genomic analysis of families with generalized vitiligo and this specific constellation of associated autoimmune disorders will be important to identify the mechanisms of genetic susceptibility to autoimmunity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12753387&dopt=Abstract [PubMed - in process]

Parasite Immunol. 2003 Jan;25(1):27-37.
Ixodes ricinus tick salivary gland extract inhibits IL-10 secretion and CD69 expression by mitogen-stimulated murine splenocytes and induces hyporesponsiveness in B lymphocytes.

Hannier S, Liversidge J, Sternberg JM, Bowman AS.

School of Biological Science (Zoology), University of Aberdeen, Aberdeen AB24 2TZ, Scotland, UK.

Tick saliva contains immunosuppressive factors allowing this blood-feeding ectoparasite to remain on hosts and enhancing pathogen transmission. In this study, we examined the modulation of mitogen-induced activation of naive murine splenocytes by the saliva and salivary gland extract (SGE) of I. ricinus ticks. We found that saliva-specific factors reduced IL-10 production by both concanavalin A (ConA) and lipopolysaccharide (LPS) stimulated splenocytes. The LPS-induced IL-10 production is 10 times more sensitive to SGE than the ConA-induced IL-10 production. Flow cytometric analysis determined that SGE particularly inhibited B (B220+) cell IL-10 production in mitogen-stimulated splenocyte preparations. Moreover, SGE reduced the early activation marker CD69 expression on ConA-activated T cells and also on B cells in presence of ConA or LPS. Annexin V and Via-probe staining demonstrated that SGE did not increase cell death in activated splenocytes and slightly decreased apoptosis in B lymphocytes. By employing assays with isolated B cells, we further showed that SGE had a direct effect on B cells and inhibited LPS-induced B cell proliferation. Taken together, our results indicate that salivary immunomodulators induce hyporesponsiveness to mitogen in both T and B cells, and that a direct B-cell inhibitory activity is present in tick saliva.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12753435&dopt=Abstract

Oral Microbiol Immunol. 2003 Jun;18(3):199-201.
Periodontal pathogens in subgingival plaque of HIV-positive subjects with chronic periodontitis.

Patel M, Coogan M, Galpin JS.

Division of Oral Microbiology, Department of Clinical Microbiology and Infectious Diseases, Faculty of Health Sciences, University of The Witwatersrand, Johannesburg, South Africa. patelmentistry.wits.ac.za

Many putative periodontal pathogens associated with periodontal disease in human immunodeficiency virus (HIV)-infected patients also occur in non-HIV-infected individuals. This study examined the prevalence of eight periodontal pathogens in HIV-positive and HIV-negative patients with chronic periodontitis using the 16s RNA polymerase chain reaction technique. The results showed a significant prevalence of Porphyromonas gingivalis and Treponema denticola among HIV-negative patients compared to HIV-positive patients. Sixty percent of the patients in both groups were colonized by five to six species. Odds ratio analysis revealed a statistically significant positive association between three of the 28 possible combinations in the HIV-positive group. They included Prevotella nigrescens/Campylobacter rectus, P. nigrescens/P. gingivalis and P. nigrescens/T. denticola. Although the prevalence of periodontal pathogens is similar in both the groups, the combination of certain periodontal pathogens may be responsible for chronic periodontitis seen in HIV-infected adults.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12753474&dopt=Abstract

Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1444-9. Epub 2003 Jan 02.
Extensive and specific responses of a eukaryote to bacterial quorum-sensing signals.

Mathesius U, Mulders S, Gao M, Teplitski M, Caetano-Anolles G, Rolfe BG, Bauer WD.

Genomic Interactions Group, Research School of Biological Sciences, Australian National University, GPO Box 475, Canberra ACT 2601, Australia.

Many bacteria use N-acyl homoserine lactone (AHL) signals to coordinate the behavior of individual cells in a local population. The successful infection of eukaryotic hosts by bacteria seems to depend particularly on such AHL-mediated "quorum-sensing" regulation. We have used proteome analysis to show that a eukaryotic host, the model legume Medicago truncatula, is able to detect nanomolar to micromolar concentrations of bacterial AHLs from both symbiotic (Sinorhizobium meliloti) and pathogenic (Pseudomonas aeruginosa) bacteria, and that it responds in a global manner by significant changes in the accumulation of over 150 proteins, 99 of which have been identified by peptide mass fingerprinting. The accumulation of specific proteins and isoforms depended on AHL structure, concentration, and time of exposure. AHLs were also found to induce tissue-specific activation of beta-glucuronidase (GUS) reporter fusions to an auxin-responsive and three chalcone synthase promoters, consistent with AHL-induced changes in the accumulation of auxin-responsive and flavonoid synthesis proteins. In addition, exposure to AHLs was found to induce changes in the secretion of compounds by the plants that mimic quorum-sensing signals and thus have the potential to disrupt quorum sensing in associated bacteria. Our results indicate that eukaryotes have an extensive range of functional responses to AHLs that may play important roles in the beneficial or pathogenic outcomes of eukaryote-prokaryote interactions.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12511600&dopt=Abstract

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