|
|
|
Coaggregation-Mediated Interactions of Streptococci and Actinomyces Detected in Initial Human Dental Plaque. Robert J. Palmer, 2003.Streptococci and actinomyces that initiate colonization of the tooth surface frequently coaggregate with each other as well as with other oral bacteria . These observations have led to the hypothesis that interbacterial adhesion influences spatiotemporal development of plaque . To assess the role of such interactions in oral biofilm formation in vivo, antibodies directed against bacterial surface components that mediate coaggregation interactions were used as direct immunofluorescent probes in conjunction with laser confocal microscopy to determine the distribution and spatial arrangement of bacteria within intact human plaque formed on retrievable enamel chips . In intrageneric coaggregation, streptococci such as Streptococcus gordonii DL1 recognize receptor polysaccharides (RPS) borne on other streptococci such as Streptococcus oralis 34 . To define potentially interactive subsets of streptococci in the developing plaque, an antibody against RPS (anti-RPS) was used together with an antibody against S . gordonii DL1 (anti-DL1) . These antibodies reacted primarily with single cells in 4-h-old plaque and with mixed-species microcolonies in 8-h-old plaque . Anti-RPS-reactive bacteria frequently formed microcolonies with anti-DL1-reactive bacteria and with other bacteria distinguished by general nucleic acid stains . In intergeneric coaggregation between streptococci and actinomyces, type 2 fimbriae of actinomyces recognize RPS on the streptococci . Cells reactive with antibody against type 2 fimbriae of Actinomyces naeslundii T14V (anti-type-2) were much less frequent than either subset of streptococci . However, bacteria reactive with anti-type-2 were seen in intimate association with anti-RPS-reactive cells . These results are the first direct demonstration of coaggregation-mediated interactions during initial plaque accumulation in vivo . Further, these results demonstrate the spatiotemporal development and prevalence of mixed-species communities in early dental plaque . Efficacy of Posaconazole in a Murine Model of Central Nervous System Aspergillosis. Jackie K. Imai, 2004.Human central nervous system (CNS) aspergillosis has >90% mortality . We compared posaconazole with other antifungals for efficacy against murine CNS aspergillosis . All tested regimens of posaconazole were equivalent to those of amphotericin B and superior in prolonging survival and reducing CFU to those of itraconazole and caspofungin and to vehicle controls . No antifungal regimen effected cure . No toxicity was noted . Overall, posaconazole shows potential for treating CNS aspergillosis . InvB Is a Type III Secretion-Associated Chaperone for the Salmonella enterica Effector Protein SopE. Sang Ho Lee, 2003.SopE is a bacteriophage-encoded effector protein of Salmonella enterica serovar Typhimurium that is translocated into the cytosol of eukaryotic cells by a type III secretion system (TTSS) (W.-D . Hardt, H . Urlaub, and J . E . Galán, Proc . Natl . Acad . Sci . USA 95:2574-2579, 1998; M . W . Wood, R . Rosqvist, P . B . Mullan, M . H . Edwards, and E . E. Galyov, Mol . Microbiol . 22:327-338, 1996) . In this study, we provide evidence that an unlinked gene carried within the Salmonella pathogenicity island 1 (SPI-1), invB (K. Eichelberg, C . Ginocchio, and J . E . Galán, J. Bacteriol . 176:4501-4510, 1994), is required for the secretion of SopE through the SPI-1 TTSS . Furthermore, far-Western blotting analysis shows that SopE directly interacts with InvB through a domain located at its amino terminus . We conclude that InvB is the TTSS-associated chaperone for SopE . Use of Real-Time Quantitative PCR for the Analysis of Merete Lunde, 2003.Bacteriophages are a common and constant threat to proper milk fermentation . It has become evident that lysogeny is widespread in lactic acid bacteria, and in this work the temperate lactococcal bacteriophage
|
© 2005
Transgalactic Ltd (manufacturer of Bioscreen C software) |
Privacy Statement | P.O. Box
1393, 00101 Helsinki, Finland,
Last modified: May 25, 2005
| ||||||