Difference between revisions of "Bifidobacterium breve"

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A Microbial Biorealm page on the genus Bifidobacterium breve


Higher order taxa

Bacteria; Actinobacteria; Actinobacteria; Bifidobacteriales; Bifidobacteriaceae; Bifidobacterium; Bifidobacterium breve


Bifidobacterium breve

NCBI: Taxonomy

Description and significance

Members of the genus Bifidobacteria are considered the most prominent colonizers of the human gastrointestinal tract subsequent to birth, representing ~25% - 80% of the cultivatable bacteria isolated from the feces of infant and adult humans [1]. Members of the species Bifidobacterium breve are anaerobic, rod-shaped, gram-positive bacterium that lack cell motility, sporulation, and a cell capsule [2]. Although B. breve have been found within the gut flora of fully grown adult humans, they are found in much higher quantities within the infant gut and were first isolated from breast-fed infant feces in 1990 [cited from 3]. B. breve have unique metabolic capabilities (see Metabolism) that underlie their importance as a dominant commensal bacterium within the gut [3]. B. breve, in particular, plays a key role in human infant metabolism of breast-milk, which contains Human Milk Oligosaccharides (HMO) indigestible by the human host. B. breve is one of three species of the genus Bifidobacterium that demonstrates probiotic capabilities. The particular species B. breve has been studied for its potential in treating childhood constipation in conjugation with Bifidobacterium bifidum and Lactobacillus acidophilus [4].

Genome structure

The species Bifidobacterium breve has a single circular [5] chromosome consisting of 2,422,684-bp with a relatively high guanine-cytosine (G+C) composition of 58.7%. The genome of B. breve is anticipated to comprise 1,985 genes, 1,854 of which are protein-coding gene sequences estimated to an average length of 1,099 bp [7]. Additionally, the B. breve genome is estimated to encompass an average 1817 Open Reading Frames (ORFs), 26% of which are, after a BLAST-based silico analysis, expected to encode hypothetical proteins. In a B. breve genome sequencing analysis [8] only one of the 8 analyzed strains was observed to contain a plasmid, thus suggesting infrequent plasmid presence within the B. breve species. B. breve are saccharolytic organisms that depend on carbohydrates present within their host’s gastrointestinal tract for their carbon and energy sources. It is estimated that ~8% of the B. breve genome is expressly devoted to metabolism of such carbohydrate sources [3]. B. breve are also particularly important within the infant gastrointestinal tract where they metabolize the sialic acid component of Human Milk Oligosaccharides (HMOs) present within the Human breast milk consumed by the infant [3]. Sialic acid is also present with human colonic mucin on the surface-exposed end [cited from 3]. In an experiment performed in 2015, 14 strains of B. breve were tested and examined for growth provided only with sialic acid as a carbon source. 11 of these strains were found capable of growth. Additionally a DNA microarray of B. breve strain UCC2003 identified 12 genes likely involved in the catabolism and uptake of sialic acid [3] The species Bifidobacterium breve (specifically strain M-16V) does not contain regions of DNA that demonstrate homology to known antibiotic resistance gene sequences present in other species of the genus Bifidobacterium or Lactobacilli [9].

Cell and colony structure

Bifidobacterium breve are non-motile, anaerobic, gram-positive bacteria. They lack the ability to form endospores and do not contain a cell capsule. Individual cells are slender, but short, club-shaped rods. Colonies of B. breve are Pulvinate to Convex and entire with diameters ranging from 2-3 mm. Colonies are smooth and assume a paste-like consistency [2].


Bifidobacterium breve and other members of the Bifidobacterium genus are fermentative bacteria that primarily form lactic and acetic acid through catabolism of carbohydrates, particularly oligosaccharides [4]. Low nutrient concentrations are rampant within the gastrointestinal tract, therefore Bifidobateria synthesize a number of unique metabolic enzymes, transporters, and glycosidases that participate in an exclusive fermentation pathway termed Bifid shunt, a fructose-6-phosphate phosphoketolase pathway, that enables catabolism of varied carbohydrates indigestible by the human or animal host [6]. Bifidobacteria are one of the initial colonizers of the infant gastrointestinal tract transferred from female parent to offspring via breast milk. Breast milk contains certain Human Milk Oligosaccharides (HMOs) that are indigestible by the infant consumer. Recently a novel metabolic pathway has been discovered with the B. breve species, titled galacto-N-biose/lacto-N-biose I, that enables catabolism of both glycoconjugates and the Human Milk Oligosaccharides (HMOs) present in the breast milk. Sialic acid is the specific component of HMOs catabolized by B. breve and the species’ genome was found to contain a gene cluster whose sole purpose is in the uptake and metabolism of the acid [3]. B. breve (strain UCC2003) has also been found capable of cross-feeding on the sialic acid produced as metabolic waste in the catabolism of 3′-sialyllactose by B. bifidum PRL2010 [3].


Bifidobacterium breve is primarily located in human breast milk and the gastrointestinal tract of infant and adult humans, where they are among the first microbial colonizers, passed from the mother to her offspring. Bifidobacterium breve exhibit a symbiotic relationship with their host by exploiting their unique metabolic capabilities in order to catabolize certain carbohydrates, such as the oligosaccharides present in human breast milk, that are indigestible by their host [5] As an individual ages the total population of Bifidobacterium breve within their gut markedly decreases. This could possibly be due in part to the lack of antibiotic resistance exhibited by B. breve, which promotes relatively easy annihilation through antibiotic usage [9]. Studies have linked the decline in B. breve population numbers to increases in the population numbers of Shiga toxin-producing Escherichia coli, thus suggesting that B. breve plays a signature role in maintaining gut micro biota homeostasis [10]. Commercial probiotics, containing B. breve, are sold in attempts to remedy the drastic decline in species population numbers by supplementing colonization. One study performed in the Netherlands, found that B. breve M-16 V may be beneficial in the treatment of chronic asthma by inducing regulatory T cell responses in lung airways of chronically asthmatic mice [11].


Bifidobacterium breve has not been recorded as the cause of human disease and has been in commercial use as a probiotic since 1976. B. breve is important within the human gut for its ability to metabolize diverse carbohydrates, breaking them down into less complex compounds digestible by the human host. Numerous controlled tests have been conducted prior to marketing in order to ensure the safety of commercial use [9].


[1] http://www.ncbi.nlm.nih.gov/pubmed/16167966 Picard, C. Fioramonti, J. Francois, A. Robinson, T. Neant, F. and Matuchansky, C. (2005) Review article: bifidobacteria as probiotic agents – physiological effects and clinical benefits, Aliment Pharmacol Ther; 22: 495-512, doi: 10.111/j.1365-2036.2005.02615.x

[2] http://ijs.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-21-4-273 Reuter, G. (1971) Designation of Type Strains for Bifidobacterium Species, Int J Syst Evol Microbiol; 21: 273-275, doi: 10.1099/00207713-21-4-273

[3] http://aem.asm.org/content/80/14/4414.full?sid=1bdf8f7b-05ec-446d-9ffc-9499b99e27c6 Egan, M. O'Connell Motherway,M. Ventura, M. and van Sinderen, M. (2014) Genetics and Molecular Biology Metabolism of Sialic Acid by Bifidobacterium breve UCC2003Appl. Environ. Microbiol 80:14, 4414-4426; doi:10.1128/AEM.01114-14

[4] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3048518/ Tabbers, MM., I de Milliano, Roseboom, MG. Benninga, MA. (2011) Is Bifidobacterium breve effective in the treatment of childhood constipation? Results from a pilot study, Nutr J; 10: 19, doi: 10.1186/1475-2891-10-19

[5] Mayo, B. (2010). Bifidobacteria: Genomics and molecular aspects (p. Xii 260). Norfolk, UK: Caister Academic.

[6] http://www.tandfonline.com/doi/pdf/10.1271/bbb.100494 Fushinobu, S. (2010). Unique Sugar Metabolic Pathways of Bifidobacteria. Bioscience, Biotechnology and Biochemistry, 74(12), 2374-2384.

[7] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155821/ Motherway, M. O'connell, A. Zomer, S. C. Leahy, J. Reunanen, F. Bottacini, M. J. Claesson, F. O'brien, K. Flynn, P. G. Casey, J. A. Moreno Munoz, B. Kearney, A. M. Houston, C. O'mahony, D. G. Higgins, F. Shanahan, A. Palva, W. M. De Vos, G. F. Fitzgerald, M. Ventura, P. W. O'toole, and D. Van Sinderen. (2011). Functional genome analysis of Bifidobacterium breve UCC2003 reveals type IVb tight adherence (Tad) pili as an essential and conserved host-colonization factor, Proc Natl Acad Scif; 108 (27): 11217-11222, doi: 10.1073/pnas.1105380108

[8] http://www.biomedcentral.com/1471-2164/15/170 Bottacini, F., Motherway, M., Kuczynski, J., O’Connell, K., Serafini, F., Duranti, S., . . . Sinderen, D. (2014). Comparative genomics of the Bifidobacterium breve taxon. BMC Genomics, 15, 170-170. doi:10.1186/1471-2164-15-170 cited in: [4]

[9] www.fda.gov/downloads/Food/IngredientsPackagingLabeling/GRAS/NoticeInventory/UCM346881

[10] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC375161/ Asahara, T., Shimizu, K., Nomoto, K., Hamabata, T., Ozawa, A., & Takeda, Y. (2004). Probiotic Bifidobacteria Protect Mice from Lethal Infection with Shiga Toxin-Producing Escherichia coli O157:H7. Infection and Immunity, 72(4), 2240-2247.

[11] Sagar, S., Morgan, M., Chen, S., Vos, A., Garssen, J., Bergenhenegouwen, J., . . . Folkerts, G. (2014). Bifidobacterium breve and Lactobacillus rhamnosus treatment is as effective as budesonide at reducing inflammation in a murine model for chronic asthma. Respiratory Research Respir Res, 15(1), 46-46. doi:10.1186/1465-9921-15-46

Edited by Katarina Weissbach of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio