Halitosis Vaccines Targeting FomA, a Biofilm-bridging Protein of Fusobacteria nucleatum
2013
Halitosis (bad breath) is estimated to influence more than half of the world's population with varying
degree of intensity. More than 85% of halitosis originates from oral bacterial infections. Foul-smelling breath
mainly results from bacterial production of volatile sulfur compounds (VSCs) such as hydrogen sulfide and
methyl mercaptan. To date, major treatments for elimination of oral malodor include periodontal therapy
combined with antibiotics or antimicrobial agents, and mechanical approaches including tooth and tongue
cleaning. These treatments may transiently reduce VSCs but carry risks of generating toxicity, increasing
resistant strains and misbalancing the resident human flora. Therefore, there is a need to develop alternative
therapeutic modalities for halitosis. Plaque biofilms are the principal source for generating VSCs which are
originally metabolized from amino acids during co-aggregation of oral bacteria. Blocking the bacterial coaggregation,
therefore, may prevent various biofilm-associated oral diseases such as periodontitis and
halitosis. Fusobacterium nucleatum (F. nucleatum), a Gram-negative anaerobe oral bacterium, is a main
bacterial strain related to halitosis. Aggregation of F. nucleatum with other bacteria to form plaque biofilms in
oral cavity causes bad breath. FomA, the major outer membrane protein of F. nucleatum, recruits other oral
pathogenic bacteria such as Porphyromonas gingivalis (P. gingivalis) in the periodontal pockets. A halitosis
vaccine targeting F. bacterium FomA significantly abrogates the enhancement of bacterial co-aggregation,
biofilms, production of VSCs, and gum inflammation mediated by an inter-species interaction of F. nucleatum
with P. gingivalis, which suggests FomA of F. nucleatum to be a potential target for development of vaccines or
drugs against bacterial biofilm formation and its associated pathogenicities.
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