| Bifidobacterium | |
|---|---|
 | |
| Bifidobacterium adolescentis | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Bacillati |
| Phylum: | Actinomycetota |
| Class: | Actinomycetes |
| Order: | Bifidobacteriales |
| Family: | Bifidobacteriaceae |
| Genus: | Bifidobacterium Orla-Jensen 1924 (Approved Lists 1980)[1] |
| Type species | |
| Bifidobacterium bifidum (Tissier 1900) Orla-Jensen 1924 (Approved Lists 1980) | |
| Species | |
See text. | |
Bifidobacterium is agenus ofgram-positive,nonmotile, often branchedanaerobicbacteria. They are ubiquitous inhabitants of thegastrointestinal tract[2][3] though strains have been isolated from thevagina[4] and mouth (B. dentium) of mammals, including humans. Bifidobacteria are one of the major genera of bacteria that make up the gastrointestinal tractmicrobiota in mammals. Some bifidobacteria are used asprobiotics.
Before the 1960s,Bifidobacterium species were collectively referred to asLactobacillus bifidus.
Underlying most of the beneficial effects ofBifidobacterium are improvedimmune system function and reduction ininflammation.[5] Notably,Bifidobacterium increasesregulatory T cells and improves the intestinal barrier.[5]Bifidobacterium produces essential metabolites for use by other key bacteria.[5]Bifidobacterium carbohydratefermentation producesacetate andbutyrate, which can protect against various diseases.[5]
In 1899,Henri Tissier, a Frenchpediatrician at thePasteur Institute in Paris, isolated a bacterium characterised by a Y-shaped morphology ("bifid") in the intestinal microbiota of breast-fed infants and named it "bifidus".[6] In 1907,Élie Metchnikoff, deputy director at the Pasteur Institute, propounded the theory thatlactic acid bacteria are beneficial to human health.[6] Metchnikoff observed that thelongevity of Bulgarians was the result of their consumption offermented milk products.[7] Metchnikoff also suggested that "oral administration of cultures of fermentative bacteria would implant the beneficial bacteria in the intestinal tract".[8]
The genusBifidobacterium possesses a uniquefructose-6-phosphate phosphoketolase pathway employed to fermentcarbohydrates.[citation needed]
Much metabolic research on bifidobacteria has focused onoligosaccharide metabolism, as these carbohydrates are available in their otherwise nutrient-limited habitats. Infant-associated bifidobacterialphylotypes appear to have evolved the ability to fermentmilk oligosaccharides, whereas adult-associated species use plant oligosaccharides, consistent with what they encounter in their respective environments. As breast-fed infants often harbor bifidobacteria-dominated gut consortia, numerous applications attempt to mimic the bifidogenic properties of milk oligosaccharides. These are broadly classified as plant-derivedfructooligosaccharides or dairy-derivedgalactooligosaccharides, which are differentially metabolized and distinct from milk oligosaccharidecatabolism.[3]
The sensitivity of members of the genusBifidobacterium to O2 generally limits probiotic activity to anaerobic habitats. Recent research has reported that someBifidobacterium strains exhibit various types ofoxic growth. Low concentrations of O2 and CO2 can have a stimulatory effect on the growth of theseBifidobacterium strains. Based on the growth profiles under different O2 concentrations, theBifidobacterium species were classified into four classes: O2-hypersensitive, O2-sensitive, O2-tolerant, andmicroaerophilic. The primary factor responsible for aerobic growth inhibition is proposed to be the production ofhydrogen peroxide (H2O2) in the growth medium. A H2O2-formingNADHoxidase was purified from O2-sensitiveBifidobacterium bifidum and was identified as ab-typedihydroorotate dehydrogenase. The kinetic parameters suggested that the enzyme could be involved in H2O2 production in highly aerated environments.[9]
Members of the genusBifidobacterium have genome sizes ranging from 1.73 (Bifidobacterium indicum) to 3.25 Mb (Bifidobacterium biavatii), corresponding to 1,352 and 2,557 predicted protein-encodingopen reading frames, respectively.[10]
Functional classification ofBifidobacterium genes, including thepan-genome of this genus, revealed that 13.7% of the identified bifidobacterial genes encode enzymes involved incarbohydrate metabolism.[10]
AddingBifidobacterium as a probiotic to conventional treatment ofulcerative colitis has been shown to be associated with improved rates of remission and improved maintenance of remission.[11] SomeBifidobacterium strains are considered as important probiotics and used in the food industry. Different species and/or strains of bifidobacteria may exert a range of beneficial health effects, including the regulation of intestinal microbialhomeostasis, the inhibition of pathogens and harmful bacteria that colonize and/or infect the gut mucosa, the modulation of local and systemic immune responses, the repression of procarcinogenic enzymatic activities within the microbiota, the production of vitamins, and the bioconversion of a number of dietary compounds into bioactive molecules.[3] Bifidobacteria improve the gut mucosal barrier and lower levels oflipopolysaccharide in the intestine.[12]
Bifidobacteria may also improve abdominal pain in patients withirritable bowel syndrome (IBS) though studies to date have been inconclusive.[13]
Naturally occurringBifidobacterium spp. may discourage the growth ofGram-negative pathogens in infants.[14]
A mother's milk contains high concentrations of lactose and lower quantities of phosphate (pH buffer). Therefore, when mother's milk is fermented by lactic acid bacteria (including bifidobacteria) in the infant's gastrointestinal tract, the pH may be reduced, making it more difficult for Gram-negative bacteria to grow.[citation needed]
The human infant gut is relatively sterile up until birth, where it takes up bacteria from its surrounding environment and its mother.[15] Themicrobiota that makes up the infant gut differs from the adult gut. An infant reaches the adult stage of their microbiome at around three years of age, when their microbiome diversity increases, stabilizes, and the infant switches over to solid foods. Breast-fed infants are colonized earlier byBifidobacterium when compared to babies that are primarily formula-fed.[16]Bifidobacterium is the most common bacteria in the infant gut microbiome.[17] There is more variability ingenotypes over time in infants, making them less stable compared to the adultBifidobacterium. Infants and children under three years old show low diversity in microbiome bacteria, but more diversity between individuals when compared to adults.[18] Reduction ofBifidobacterium and increase in diversity of the infant gut microbiome occurs with less breast-milk intake and increase of solid food intake. Mammalian milk all containoligosaccharides showing natural selection.[clarification needed] Human milk oligosaccharides are not digested by enzymes and remain whole through the digestive tract before being broken down in the colon by microbiota.Bifidobacterium species genomes ofB. longum, B. bifidum,B. breve contain genes that can hydrolyze some of the human milk oligosaccharides and these are found in higher numbers in infants that are breast-fed.Glycans that are produced by the humans are converted into food and energy for theB. bifidum. showing an example ofcoevolution.[19]
The genusBifidobacterium comprises the following species:[20]
Bombiscardovia Group (all cultured from the hindgut of bees)
Bifidobacterium adolescentis Group
Bifidobacterium bifidium Group
Bifidobacterium bombi Group (Milk and Honey)
Bifidobacterium boum Group
Bifidobacterium longum Group
Bifidobacterium pullorum Group (from birds and rabbits)
Bifidobacterium pseudolongum Group
Bifidobacterium psychroarophilum Group
Bifidobacterium tissieri Group (from primates)
Ungrouped Bifidobacterium
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