Faecalibacterium is a genus of bacteria. The genus contains several species includingFaecalibacterium prausnitzii,Faecalibacterium butyricigenerans,Faecalibacterium longum,[1]Faecalibacterium duncaniae,Faecalibacterium hattorii, andFaecalibacterium gallinarum.[2] Its first known species,Faecalibacterium prausnitzii (renamed as Faecalibacteriumduncaniae) is gram-positive,[3] mesophilic, rod-shaped,[3] and anaerobic,[4] and is one of the most abundant and importantcommensal bacteria of the humangut microbiota. It is non-spore forming and non-motile.[5] These bacteria producebutyrate and othershort-chain fatty acids through the fermentation ofdietary fiber. The production ofbutyrate makes them an important member of the gut microbiota, fighting againstinflammation.[6]
Formerly assigned to the genusFusobacterium in thephylumFusobacteriota,Faecalibacterium prausnitzii was re-assigned to its own genus when phylogenetic analysis of isolates showed it to be a member of the phylumBacillota. It now is regarded as a member of theOscillospiraceae inClostridium cluster IV.[7] Although the Oscillospiraceae are largelygram-negative bacteria,Faecalibacterium prausnitzii resembles agram-positive bacterium in its staining.[8] This can be ascribed to the fact that it lacks lipopolysaccharides in its outer membrane, so that, in its staining, it more closely resembles gram-positive bacteria, than gram-negative.
Faecalibacterium prausnitzii has a genome 2,868,932 bp long and has aGC-content of 56.9%. The bacterium has been found to have 2,707 coding sequences, including 77 RNAs encoding genes.[5] 128 metabolic pathways have been reconstructed, as well as 27 protein complexes and 64 tRNAs.[17] Phylogenetically, the strains ofF. prausnitzii composephylogroups I and II. Most of the new isolates of this species isolated by Muhammad Tanweer Khan belong to phylogroup II.[18] A protein produced by this bacterium has been linked to anti-inflammatory effects.[19]
Faecalibacterium prausnitzii in laboratory conditions
Faecalibacterium prausnitzii is strictlyanaerobic, and accordingly difficult to culture in the laboratory. However, with due attention to the requisite conditions and media, it is possible to culture the speciesin vitro. The rich medium YCFA is very suitable for the growth of this bacterium in anaerobic conditions.[20] Another media suitable for the growth of F. prausnitzii is YBHI.[20] Any liquid media or agar plates should be pretreated beforehand for 24 hours in an anaerobic chamber, to ensure they are completely anaerobic.
In healthy adults,Faecalibacterium prausnitzii represent approximately 5% of the total fecal microbiota but this can increase to around 15% in some individuals, making it one of the commonest of the gut bacteria.[8] The anti-inflammatory properties of itsmetabolites may alleviate imbalances between intestinal bacterial populations that lead todysbiosis.[8] It is one of the main producers of butyrate in the intestine. Sincebutyrate inhibits the production ofNF-kB andIFN-y, both involved in the pro-inflammatory response,Faecalibacterium prausnitzii acts as an anti-inflammatory gut bacterium.[21][22][23] By blocking theNF-kB pathway,F. prausnitzii indirectly inhibts the production of the pro-inflammatoryIL-8, secreted by theintestinal epithelial cells.[24] Other research has shown that there is a correlation between high populations ofFaecalibacterium prausnitzii, lowIL-12 abundance, and higherIL-10 production.[25][26] The upregulated IL-10 inhibts the secretion ofIFN-y,TNF-alpha,IL-6, andIL-12, which are allpro-inflammatory cytokines.[26] Apart from butyrate,F. prausnitzii produceformate andD-lactate as byproducts of fermentation of glucose and acetate.[21][7] Lower than usual levels ofF. prausnitzii in the intestines have been associated withCrohn's disease,obesity,asthma andmajor depressive disorder.[26][27][28][29] Higher than usual levels of the F06clade ofF. prausnitzii have been associated withatopic dermatitis.[30]Faecalibacterium prausnitzii can improvegut barrier function.[31] Supernatant ofF. prausnitzii has been shown to improve the gut barrier by affecting the permeability of epithelial cells.[32] Another way thatF. prausnitzii improves the gut barrier is by improving the permeability and the expression of tightly bound proteins -e-cadherin andoccludin. Both of them increase thetight junctions between cells, strengthen the gut barrier and alleviate inflammation.[33][21]
Studies show thatF. prausnitzii interacts with other bacteria, which affects its butyrate production, and survival. WhenF. prausnitzii is cultured withBacteroides thetaiotaomicron, it produces more butyric acid than standing alone,[34][20]F. prausnitzii also benefits from growing with certain other bacteria. For example, in order to survive in the gut environment, it requires certain bacteria to be preexisting.B. thetaiotaomicron andEscherichia coli are needed to create a suitable environment forF. prausnitzii by reducing the redox potential and alter the composition of the nutrients.[35][20]
In Crohn's disease, as of 2015 most studies (with one exception) found reduced levels ofF. prausnitzii;[36] this has been found in both fecal and mucosal samples.[37] The lower abundance of these bacteria is not only associated to the chance of developingIBD, but also to the chance of relapsing after a successful therapy. People with lower abundance are six times more likely to relapse in the future.[26] However, it is afastidious organism sensitive to oxygen and difficult to deliver to the intestine.[37]
Exclusiveenteral nutrition, which is known to induce remission in Crohn's, has been found to reduceF. prausnitzii in responders.[38] This could be due to the lack of specific nutrients, that the bacteria need to survive.[39]
F. prausnitzii can also serve as a biomarker discriminating between different intestinal inflammatory conditions. It is a good biomarker to differentiate betweenCrohn's disease andcolorectal cancer.[40] An even better biomarker isF. prausnitzii in comparison toE. coli as a complementary indicator (F-E index). This index serves really well in differentiating between colorectal cancer andulcerative colitis.[40]
Combining both the host serological data plus microbiological indicators could serve as good biomarker, since it has been reported that Crohn's disease and ulcerative colitis can be differentiated based on monitoring ofF. prausnitzii in conjunction withleukocyte count.[41]
^Stenman LK, Burcelin R, Lahtinen S (February 2016). "Establishing a causal link between gut microbes, body weight gain and glucose metabolism in humans - towards treatment with probiotics".Beneficial Microbes.7 (1):11–22.doi:10.3920/BM2015.0069.PMID26565087.
