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Chenggang Wu

Chenggang Wu

Regular Member

Assistant Professor

[email protected]
MSB 1.618

The University of Texas Health Science Center at Houston
McGovern Medical School
Department of Microbiology and Molecular Genetics

Fusobacterium nucleatum is an oral pathobiont not only associated with periodontitis, but also with extra-oral disease such as preterm birth and colorectal cancer. Our current study is focused on understanding the regulations that control F. nucleatum-mediated coaggregation. Coaggregation, defined as formation of aggregates caused by cell-to-cell recognition of genetically distinct bacteria via the interactions between adhesins and their cognate complementary receptors, is an important driving force for multispecies biofilm formation in nature. F. nucleatum is a prominent colonizer in dental plaque and has an outstanding coaggregation ability. F. nucleatum exhibits coaggregation with nearly all tested oral bacteria. Because of this, F. nucleatum has been proposed as a bridge microorganism in dental plaque by virtue of its coaggregation with early and late colonizers. In the past decades, intensive works have been done to find what bacteria can aggregate with F. nucleatum and what adhesins in F. nucleatum are responsible for their coaggregation. Studies of coaggregation have so far yielded four fusobacterial adhesins, RadD, CmpA, FomA and Fap2.  Of these, FomA and Fap2 bind Porphyromonas gingivalis, CmpA binds a specific Streptococcus strain, and RadD, a versatile adhesin, mediates fusobacterial aggregation with many early and late colonizers, including Aggregatibacter actinomycetemcomitans. Vital for plaque development, this RadD-mediated coaggregation process is an excellent experimental model to study various cell-cell interactions within dental plaque. Theoretically, expression of adhesins in F. nucleatum should be tightly regulated since increasing surface adhesins promotes oral biofilm formation, and reducing their levels results in bacterial dispersal, which change the diversity and composition of dynamic dental plaque and probably shift a health-associated plaque to a pathogenic one. However, little known about the regulatory mechanisms underlying the multispecies interactions involving F. nucleatum.


McGovern Medical School Faculty

Wu Lab

Education & Training

PhD, Institute of Microbiology, 2007