Faecalibacterium prausnitzii
Species of bacterium
From Wikipedia, the free encyclopedia
Faecalibacterium prausnitzii is a non-spore-forming, non-motile, rod-shaped, anaerobic, Gram-positive bacteria species of the genus Faecalibacterium.[1][2][3] It found in the human gut and is the most abundant single bacteria species in the human gut microbiota, making up approximately 5% of the total bacterial population in healthy adults.[1][2][3] However, F. prausnitzii can make up as much as 15% of the bacterial population in some people.[1] Many different strains of F. prausnitzii with varying properties are known and have been studied.[4][5][6][7]
| Faecalibacterium prausnitzii | |
|---|---|
| |
| Fusobacterium prausnitzii under scanning electron microscope. | |
Scientific classification  | |
| Domain: | Bacteria |
| Kingdom: | Bacillati |
| Phylum: | Bacillota |
| Class: | Clostridia |
| Order: | Eubacteriales |
| Family: | Oscillospiraceae |
| Genus: | Faecalibacterium |
| Species: | F. prausnitzii |
| Binomial name | |
| Faecalibacterium prausnitzii (Hauduroy et al. 1937) Duncan et al. 2002 | |
| Synonyms | |
|
Bacteroides prausnitzii | |
F. prausnitzii is an extremely oxygen-sensitive bacteria and is difficult to cultivate even under oxygen-free conditions.[1][2] However, advances have been made in the cultivation of F. prausnitzii.[1][3] The end products of glucose fermentation by F. prausnitzii include acetate (acetic acid), formate, small amounts of D-lactate, and substantial amounts of butyrate (butyric acid).[1][2] It also consumes acetate and forms butyrate from it.[3][8] Salicylic acid is another product of F. prausnitzii.[2][3] F. prausnitzii is the most important butyrate-producing bacteria in the gut and colon.[2][1][9] Butyrate is a short-chain fatty acid and has a large variety of biological effects.[1][10] It is an agonist of the FFAR2 (GPR43), FFAR3 (GPR41), and GPR109A and a histone deacetylase (HDAC) inhibitor of HDAC classes I and II.[10] It is known to activate the brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) signaling pathway via its HDAC inhibition and produce associated effects.[11][12] In addition to its mechanistic actions, butyrate is the preferred energy source for colonocytes, and has been found to provide approximately 70% of total energy needs for colonocytes in mice.[10] Butyrate plays a key role in gut homeostasis and has anti-inflammatory effects among others.[10]
F. prausnitzii abundance has been inversely associated with inflammatory bowel diseases such as Crohn's disease and ulcerative colitis.[2][1][10] It has also been inversely associated with colorectal cancer and other diseases.[2][3] In the 2020s, it was found that F. prausnitzii is depleted in people with systemic lupus erythematosus (SLE; "lupus"), and that its restoration could improve symptoms of the disease in animal models.[13][9][7] One possible mechanism for these apparent benefits is increased butyrate production.[14][15][16] Reduced Faecalibacterium prausnitzii abundance and butyrate production has been associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID and in the case of ME/CFS this has been assessed and found to correlate with fatigue severity as well.[17][18][19][20]
Prebiotics like fiber (e.g., inulin) have been found to increase F. prausnitzii abundance.[3][21][22] The short-chain triglyceride triacetin (glycerol triacetate) may also increase F. prausnitzii abundance by providing acetate.[23][3][8] Tributyrin (glycerol tributyrate) directly converts into butyrate and has additionally been found to increase butyrate-producing bacteria, though effect on F. prausnitzii specifically has not been reported.[24][25][26][27][28] Probiotics do not contain F. prausnitzii, but some may nonetheless increase its abundance via increased acetate production.[3][7] Various medications have been found to increase or reverse depletion of F. prausnitzii concentrations, such as the antibiotic rifaximin, interferon α-2b, high-dose hydrocortisone, and the TNF inhibitor infliximab.[1][2][29] Another means of increasing F. prausnitzii abundance is fecal microbiota transplant (FMT).[3] Antibiotics such as amoxicillin and ciprofloxacin have been found to decrease Faecalibacterium species, whereas nitrofurantoin increased them.[3][30][31] As of 2021, there has been very little research into the role of short chain fatty acid-producing bacteria and potential therapeutic benefits in inflammatory bowel disease.[32] However, F. prausnitzii supplementation is now being studied in clinical trials for certain indications.[3] There are challenges to F. prausnitzii manufacturing and administration due to its oxygen sensitivity among other issues.[3]
F. prausnitzii was discovered by C. Prausnitz in 1922.[3][33] It was initially classified as Bacteroides prausnitzii in 1937 by P. Hauduroy and colleagues.[3][34] Subsequently, the bacteria was reclassified as Fusobacterium prausnitzii in 1974.[3][1][35] In 1996 however, genetic analysis revealed that F. prausnitzii is only distantly related to Fusobacterium.[1] Later, a new genus called Faecalibacterium was proposed and the species was renamed to Faecalibacterium prausnitzii in 2002.[1][3] Relatedly, F. prausnitzii was the first member of Faecalibacterium to be discovered.[3] The first complete genome of F. prausnitzii was sequenced in 2010 in the frame of the Human Microbiome Project.[1] F. prausnitzii has received very little scientific attention until around the 2010s, probably in part due to its extreme oxygen sensitivity and cultivation difficulties.[1][2][3]