Letters to Nature
Nature 417, 552-555 (30 May 2002) | doi:10.1038/417552a; Received 5 December 2001; Accepted 14 March 2002
A component of innate immunity prevents bacterial biofilm development
Pradeep K. Singh1, Matthew R. Parsek2, E. Peter Greenberg3,4 and Michael J. Welsh1,4,5
- Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA
- Department of Microbiology, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA
- Department of Physiology and Biophysics and Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA
- Department of Civil Engineering, Northwestern University, Evanston, Illinois 60208, USA
- W. M. Keck Foundation Microbial Communities and Cell Signaling Laboratory, Iowa City, Iowa 52242, USA
Correspondence to: Pradeep K. Singh1 Correspondence and requests for materials should be addressed to P.K.S. (e-mail: Email: pradeep-singh@uiowa.edu).
Antimicrobial factors form one arm of the innate immune system, which protects mucosal surfaces from bacterial infection1, 2, 3. These factors can rapidly kill bacteria deposited on mucosal surfaces and prevent acute invasive infections1, 2, 3, 4. In many chronic infections, however, bacteria live in biofilms, which are distinct, matrix-encased communities specialized for surface persistence5, 6, 7. The transition from a free-living, independent existence to a biofilm lifestyle can be devastating, because biofilms notoriously resist killing by host defence mechanisms and antibiotics5, 8. We hypothesized that the innate immune system possesses specific activity to protect against biofilm infections. Here we show that lactoferrin, a ubiquitous and abundant constituent of human external secretions, blocks biofilm development by the opportunistic pathogen Pseudomonas aeruginosa. This occurs at lactoferrin concentrations below those that kill or prevent growth. By chelating iron, lactoferrin stimulates twitching, a specialized form of surface motility, causing the bacteria to wander across the surface instead of forming cell clusters and biofilms. These findings reveal a specific anti-biofilm defence mechanism acting at a critical juncture in biofilm development, the time bacteria stop roaming as individuals and aggregate into durable communities.