English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Denitrification in human dental plaque

MPS-Authors
/persons/resource/persons210762

Schreiber,  F.
Department of Biogeochemistry, Max Planck Institute for Marine Microbiology, Max Planck Society;

/persons/resource/persons56955

Stief,  P.
Permanent Research Group Microsensor, Max Planck Institute for Marine Microbiology, Max Planck Society;

/persons/resource/persons210399

Gieseke,  A.
Permanent Research Group Microsensor, Max Planck Institute for Marine Microbiology, Max Planck Society;

/persons/resource/persons210447

Heisterkamp,  I. M.
Permanent Research Group Microsensor, Max Planck Institute for Marine Microbiology, Max Planck Society;

/persons/resource/persons210257

de Beer,  D.
Permanent Research Group Microsensor, Max Planck Institute for Marine Microbiology, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)

Schreiber10.pdf
(Publisher version), 2MB

Supplementary Material (public)
There is no public supplementary material available
Citation

Schreiber, F., Stief, P., Gieseke, A., Heisterkamp, I. M., Verstraete, W., de Beer, D., et al. (2010). Denitrification in human dental plaque. BMC Biology, 8: 12. 1.


Cite as: https://hdl.handle.net/21.11116/0000-0001-CACE-4
Abstract
Background

Microbial denitrification is not considered important in human-associated microbial communities. Accordingly, metabolic investigations of the microbial biofilm communities of human dental plaque have focused on aerobic respiration and acid fermentation of carbohydrates, even though it is known that the oral habitat is constantly exposed to nitrate (NO3-) concentrations in the millimolar range and that dental plaque houses bacteria that can reduce this NO3- to nitrite (NO2-).
Results

We show that dental plaque mediates denitrification of NO3- to nitric oxide (NO), nitrous oxide (N2O), and dinitrogen (N2) using microsensor measurements, 15N isotopic labelling and molecular detection of denitrification genes. In vivo N2O accumulation rates in the mouth depended on the presence of dental plaque and on salivary NO3- concentrations. NO and N2O production by denitrification occurred under aerobic conditions and was regulated by plaque pH.
Conclusions

Increases of NO concentrations were in the range of effective concentrations for NO signalling to human host cells and, thus, may locally affect blood flow, signalling between nerves and inflammatory processes in the gum. This is specifically significant for the understanding of periodontal diseases, where NO has been shown to play a key role, but where gingival cells are believed to be the only source of NO. More generally, this study establishes denitrification by human-associated microbial communities as a significant metabolic pathway which, due to concurrent NO formation, provides a basis for symbiotic interactions.