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Applied and Environmental Microbiology, January 2006, p. 239-244, Vol. 72, No. 1
0099-2240/06/$08.00+0     doi:10.1128/AEM.72.1.239-244.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Effects of Lactococcus lactis on Composition of Intestinal Microbiota: Role of Nisin

Nete Bernbom,1 Tine Rask Licht,1* Carl-Henrik Brogren,2,{dagger} Birthe Jelle,3 Anette H. Johansen,2,{ddagger} Iker Badiola,2,§ Finn K. Vogensen,2 and Birgit Nørrung1

Department of Microbiological Food Safety, Danish Institute for Food and Veterinary Research, Mørkhøj Bygade 19, DK-2860 Søborg, Denmark,1 Department of Food Science, The Royal Veterinary and Agricultural University, Rolighedsvej 30, KVL, DK-1870 Frederiksberg C, Denmark,2 Department of Meat and Food Safety, Chr. Hansen A/S, Bøge Allé 2, DK-2970 Hørsholm, Denmark3

Received 13 September 2005/ Accepted 28 October 2005

This study examined the ability of (i) pure nisin, (ii) nisin-producing Lactococcus lactis strain CHCC5826, and (iii) the non-nisin-producing L. lactis strain CHCH2862 to affect the composition of the intestinal microbiota of human flora-associated rats. The presence of both the nisin-producing and the non-nisin-producing L. lactis strains significantly increased the number of Bifidobacterium cells in fecal samples during the first 8 days but decreased the number of enterococci/streptococci in duodenum, ileum, cecum, and colon samples as detected by selective cultivation. No significant changes in the rat fecal microbiota were observed after dosage with nisin. Pearson cluster analysis of denaturing gradient gel electrophoresis profiles of the 16S rRNA genes present in the fecal microbial population revealed that the microbiota of animals dosed with either of the two L. lactis strains were different from that of control animals dosed with saline. However, profiles of the microbiota from animals dosed with nisin did not differ from the controls. The concentrations of nisin estimated by competitive enzyme-linked immunosorbent assay (ELISA) were approximately 10-fold higher in the small intestine and 200-fold higher in feces than the corresponding concentrations estimated by a biological assay. This indicates that nisin was degraded or inactivated in the gastrointestinal tract, since fragments of this bacteriocin are detected by ELISA while an intact molecule is needed to retain biological activity.

* Corresponding author. Mailing address: Department of Microbiological Food Safety, Danish Institute for Food and Veterinary Research, Mørkhøj Bygade 19, DK-2860 Søborg, Denmark. Phone: 4572346000. Fax: 4572347001. E-mail: trl{at}dfvf.dk

{dagger} Present address: Department of Medical Biochemistry and Genetics, Faculty of Health, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark.

{ddagger} Present address: Department of Genomics & Strain Development, Chr. Hansen A/S, Bøge Allé 10-12, DK-2970 Hørsholm, Denmark.

§ Present address: Department of Cell Biology, Faculty of Medicine, University of The Basque Country, B Sarriena, 48940 Leioa Bizkaia, Spain.

Applied and Environmental Microbiology, January 2006, p. 239-244, Vol. 72, No. 1
0099-2240/06/$08.00+0     doi:10.1128/AEM.72.1.239-244.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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