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author:("Shi, wenchuan")
1.  Characterization of aid1, a novel gene involved in Fusobacterium nucleatum interspecies interactions 
Microbial ecology  2014;68(2):379-387.
The oral opportunistic pathogen Fusobacterium nucleatum is known to interact with a large number of different bacterial species residing in the oral cavity. It adheres to a variety of Gram-positive bacteria, including oral streptococci via the arginine-inhibitable adhesin RadD. In this study, we describe a novel protein encoded by the predicted open reading frame FN1253 that appears to play a role in interspecies interactions of F. nucleatum, particularly with oral streptococci and related Gram-positive species. We designated FN1253 as aid1 (Adherence Inducing Determinant 1). Expression analyses demonstrated that this gene was induced in F. nucleatum single species biofilms, while the presence of representative members of the oral microbiota known to adhere to F. nucleatum triggered its suppression. Inactivation as well as overexpression of aid1 affected the ability of F. nucleatum to coaggregate with oral streptococci and the closely related Enterococcus faecalis, but not other Gram-positive oral species tested. Furthermore, overexpression of aid1 led to a drastic change in the structure of dual species biofilms of F. nucleatum with oral streptococci. Aid1 function was abolished in the presence of arginine and found to be dependent on RadD. Interestingly, differential expression of aid1 did not affect mRNA and protein levels of RadD. These findings indicate that RadD-mediated adhesion to oral streptococci involves more complex cellular processes than the simple interaction of adhesins on the surface of partner strains. Aid1 could potentially play an important role in facilitating RadD-mediated interaction with oral streptococci by increasing binding specificity of F. nucleatum to other microbial species.
doi:10.1007/s00248-014-0400-y
PMCID: PMC4104215  PMID: 24643713
F. nucleatum; oral streptococci; interspecies interaction; RadD
2.  Killing of Escherichia coli by Myxococcus xanthus in Aqueous Environments Requires Exopolysaccharide-dependent Physical Contact 
Microbial ecology  2013;66(3):630-638.
Nutrient or niche-based competition among bacteria is a widespread phenomenon in natural environment. Such inter-species interactions are often mediated by secreted soluble factors and/or direct cell–cell contact. As ubiquitous soil bacteria, Myxococcus species are able to produce a variety of bioactive secondary metabolites to inhibit the growth of other competing bacterial species. Meanwhile, Myxococcus sp. also exhibit sophisticated predatory behavior, an extreme form of competition that is often stimulated by close contact with prey cells and largely depends on the availability of solid surfaces. Myxococcus sp. can also be isolated from aquatic environments. However, studies focusing on the interaction between Myxococcus and other bacteria in such environments are still limited. In this study, using the well-studied M. xanthus DK1622 and E. coli as model interspecies interaction pair, we demonstrated that in a aqueous environment, Myxococcus xanthus was able to kill Escherichia coli in a cell contact-dependent manner, and that the observed contact dependent killing required the formation of co-aggregates between M. xanthus and E. coli cells. Further analysis revealed that exopolysaccharide (EPS), type IV pilus (TFP) and lipopolysaccharide (LPS) mutants of M. xanthus displayed various degrees of attenuation in E. coli killing, and it correlated well with the mutants' reduction in EPS production. In addition, M. xanthus showed differential binding ability to different bacteria, and bacterial strains unable to co-aggregate with M. xanthus can escape the killing, suggesting the specific nature of co-aggregation and the targeted killing of interacting bacteria. In conclusion, our results demonstrated EPS mediated, contact-dependent killing of E. coli by M. xanthus, a strategy that might facilitate the survival of this ubiquitous bacterium in aquatic environments.
doi:10.1007/s00248-013-0252-x
PMCID: PMC3931608  PMID: 23828520
M. xanthus; contact-dependent interaction; co-aggregation; aqueous environment
3.  In vitro communities derived from oral and gut microbial floras inhibit the growth of bacteria of foreign origins 
Microbial ecology  2010;60(3):665-676.
The gastrointestinal (GI) tract is home to trillions of microbes. Within the same GI tract substantial differences in the bacterial species that inhabit the oral cavity and intestinal tract have been noted. While the influence of host environments and nutritional availability in shaping different microbial communities is widely accepted, we hypothesize that the existing microbial flora also plays a role in selecting the bacterial species that are being integrated into the community. In this study, we used cultivable microbial communities isolated from different parts of the GI tract of mice (oral cavity and intestines) as a model system to examine this hypothesis. Microbes from these two areas were harvested and cultured using the same nutritional conditions, which led to two distinct microbial communities, each with about 20 different species as revealed by PCR-DGGE analysis. In vitro community competition assays showed that the two microbial floras exhibited antagonistic interactions towards each other. More interestingly, all the original isolates tested and their closely related species displayed striking community preferences: they persisted when introduced into the bacterial community of the same origin, while their viable count declined more than 3 orders of magnitude after 4 days of coincubation with the microbial flora of foreign origin. These results suggest that an existing microbial community might impose a selective pressure on incoming foreign bacterial species independent of host selection. The observed inter-flora interactions could contribute to the protective effect of established microbial communities against the integration of foreign bacteria to maintain the stability of the existing communities.
doi:10.1007/s00248-010-9711-9
PMCID: PMC2954289  PMID: 20625712
4.  Oral-derived bacterial flora defends its domain by recognizing and killing intruders---- a molecular analysis using Escherichia coli as a model intestinal bacterium 
Microbial ecology  2010;60(3):655-664.
Within the same human gastrointestinal (GI) tract, substantial differences in the bacterial species that inhabit oral cavity and intestinal tract have been noted. Previous research primarily attributed the differences to the influences of host environments and nutritional availabilities (“host habitat” effect). Our recent study indicated that, other than the host habitat effect, an existing microbial community could impose a selective pressure on incoming foreign bacterial species independent of host-mediated selection (“community selection” effect). In this study, we employed in vitro microbial floras representing microorganisms that inhabit the oral cavities and intestinal tract of mice in combination with Escherichia coli as a model intestinal bacterium and demonstrated that E. coli displays a striking community preference. It thrived when introduced into the intestinal microbial community, and survived poorly in the microbial flora of foreign origin (oral community). A more detailed examination of this phenomenon showed that the oral community produced oxygen free radicals in the presence of wild type E. coli while mutants deficient in lipopolysaccharides (LPS) did not trigger significant production of these cell damaging agents. Furthermore, mutants of E. coli defective in the oxidative stress response experienced a more drastic reduction in viability when co-cultivated with the oral flora, while the exogenous addition of the anti-oxidant vitamin C was able to rescue it. We concluded that the oral-derived microbial community senses the E. coli LPS and kills the bacterium with oxygen free radicals. This study reveals a new mechanism of community invasion resistance employed by established microflora to defend their domains.
doi:10.1007/s00248-010-9708-4
PMCID: PMC2954290  PMID: 20625713

Results 1-4 (4)