Enterococcus faecalis: the pathway in the body

Enterococcus faecalis is part of the pathway “Gut bacteria”. This page shows the whole pathway; the station of Enterococcus faecalis is highlighted.

Where this laboratory value sits: Enterococcus faecalis — lactic acid bacterium. Enterococcus faecalis lives in small numbers in the gut. It grows with and without oxygen, tolerates bile and salt and ferments sugars almost entirely to lactic acid (lactate). It is naturally insensitive to cephalosporins. Source 11

In brief

Gut bacteria such as bifidobacteria, lactobacilli, Faecalibacterium and Akkermansia live mainly in the large intestine. They ferment dietary fibre and mucus sugars into short-chain fatty acids such as acetate, propionate and butyrate, which gut cells use as fuel and signal.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

1. Dietary fibre → Lactate and acetate Glycosidases Bacterial glycosidases split the long chains into sugar units; fermentation yields lactic acid, acetate and gases. Other species absorb these intermediates. Source 1, 2↑ supplies Lactate and acetate are intermediates that bacteria pass among themselves: butyrate producers absorb acetate, and lactate users turn lactate into butyrate or propionate. established physiology Source 1, 2
   ⚖ When the balance tips

   too much — If more lactate is left over than the lactate users can absorb, it accumulates in the gut contents and lowers the pH.

   too little — If little acetate is present, butyrate producers such as Faecalibacterium have less starting material for the final step.

   observed in studies · Source 1, 5

2. Lactate and acetate → Butyrate Butyryl-CoA transf. Butyrate producers use acetate and lactate from their neighbours; this handing-on is called cross-feeding. The enzyme butyryl-CoA:acetate CoA-transferase carries out the final step. If little acetate is present, less butyrate is formed. Source 1, 5↑ supplies Butyrate is the end product of cross-feeding and supplies fuel to the colon cells. A monocarboxylate transporter carries it into the cell. established physiology Source 3, 1
   ⚖ When the balance tips

   too much — If more butyrate is present than the colon cells burn, part of it reaches the liver via the portal vein.

   too little — If little butyrate is present, for example because little acetate and lactate are passed on, less of it reaches the gut wall.

   established physiology · Source 3, 1, 5

3. Butyrate → Gut wall cells β-oxidation · MCT transporter The cells of the colonic lining absorb butyrate and burn it in their mitochondria. It covers a large part of their energy needs. Butyrate left over acts as a signal in the nucleus. Source 3, 1↑ supplies In the colon cells, butyrate is turned into energy via β-oxidation. What is not burned inhibits histone deacetylases in the cell nucleus and so changes which genes are read. observed in studies Source 3
   ⚖ When the balance tips

   too much — If more butyrate is left in the cell than it burns, it inhibits histone deacetylases more strongly and alters the reading of genes. This is described mainly in cell culture.

   too little — If little butyrate arrives, the colon cells burn less of it and rely more on other fuels.

   observed in studies · Source 3, 1

4. Mucus (mucin) → Acetate and propionate Mucin glycosidases Breaking down the mucin sugar chains produces acetate and propionate. Other species nearby make further use of these substances. Propionate is used mainly in the liver. Source 4, 1↑ supplies Acetate and propionate enter the blood: propionate is used mainly in the liver, while acetate also reaches other tissues. Via FFAR2 and FFAR3 both also act as signals. established physiology Source 3, 1
   ⚖ When the balance tips

   too much — If a lot of acetate and propionate is formed, the pH of the gut contents drops, and more of them reaches the liver via the portal vein.

   too little — If little of them is formed, FFAR2 and FFAR3 are occupied less often, and butyrate producers receive less acetate.

   established physiology · Source 3, 1

5. Acetate and propionate → FFAR2 and FFAR3 Acetate and propionate bind to the receptors FFAR2 and FFAR3 on gut, fat and immune cells. Through them they act as signalling molecules, not just as fuel. Occupied receptors trigger the release of gut hormones. Source 3↑ supplies Occupied FFAR2 and FFAR3 trigger signals in the cell: hormone-producing gut cells release GLP-1 and PYY, and immune cells change their response. Much of this comes from animal models. observed in studies Source 3
   ⚖ When the balance tips

   too much — If many receptors are occupied, the hormone-producing gut cells release more GLP-1 and PYY. This is described mainly in animal models and cell culture.

   too little — If the receptors are rarely occupied, these signals become weaker; mice without FFAR2 or FFAR3 show altered hormone and immune responses.

   observed in studies · Source 3

Further stations

• Ingested bacteria — from food or preparations Strains ingested with foods or preparations, often Lactobacillus and Bifidobacterium, pass through the stomach and small intestine. Like resident species they form lactate and acetate. How long they remain detectable differs between people. Source 10, 9, 2↑ supplies Ingested strains supply lactate and acetate in the gut for as long as they are active there. Whether they settle in the mucosa depends on the resident bacterial community and differs between people. observed in studies Source 10, 9, 2
  ⚖ When the balance tips

  too much — If many bacteria of one strain arrive, it is temporarily more often detectable in the stool; the resident species can push it out of the mucosa again.

  too little — If few ingested bacteria arrive, they contribute little to fermentation; lactate and acetate then come from the resident species.

  observed in studies · Source 9, 2

• Bifidobacterium — Bifidobacteria Bifidobacteria break down dietary fibre with their own enzymes and ferment the building blocks via a special route, the bifid shunt. They pass their acetate and lactate on to butyrate producers. Source 2↑ supplies Via the bifid shunt with the enzyme phosphoketolase, bifidobacteria form acetate and lactate from sugars. They pass these substances on to butyrate producers nearby. established physiology Source 2, 6
  ⚖ When the balance tips

  too much — If many bifidobacteria are active, more acetate and lactate are formed; butyrate producers nearby then have more starting material. This has been shown mainly in mixed cultures.

  too little — If few bifidobacteria are present, less acetate is formed by this route; other species carry out part of the fibre fermentation.

  observed in studies · Source 2, 1

• Lactobacillus — Lactic acid bacteria Lactobacilli ferment sugars into lactic acid. Lactic acid lowers the pH of the gut contents and serves other bacteria as a starting material. If lactate builds up, the pH drops further. Source 1, 3↕ both, depending on amount Lactic acid acts in two directions: it lowers the pH of the gut contents, which slows some species, and it is food for lactate-using bacteria that turn it into butyrate or propionate. observed in studies Source 1, 3
  ⚖ When the balance tips

  too much — If lactate builds up because the lactate users cannot keep pace, the pH drops further; this also slows the lactate users themselves, and even more lactate is left over.

  too little — If little lactate is present, lactate users have less starting material, and less butyrate and propionate are formed by this route.

  observed in studies · Source 1

• Faecalibacterium — F. prausnitzii This bacterium uses acetate and sugar residues to form butyrate. It lives strictly without oxygen and is one of the most common species in the colon. Its butyrate is fuel for the colon cells. Source 5, 2↑ supplies Faecalibacterium absorbs acetate and supplies butyrate, the preferred fuel of colon cells. For the final step it needs acetate from its neighbours. established physiology Source 5, 2
  ⚖ When the balance tips

  too much — If many butyrate producers are active, they use up more acetate and deliver more butyrate to the gut wall.

  too little — If few butyrate producers are present, less butyrate is formed; more acetate stays in the gut contents, and the colon cells receive less of their preferred fuel.

  established physiology · Source 5, 1, 3

• Dietary fibre — indigestible carbohydrates Fibre passes through the small intestine unchanged because human enzymes cannot break its bonds. In the colon it meets bacteria that can. It is turned into short-chain fatty acids. Source 3↑ supplies Dietary fibre is the food of colonic bacteria. Fermentation turns it into acetate, propionate and butyrate as well as gases. established physiology Source 3
  ⚖ When the balance tips

  too much — If a lot of fibre arrives, more short-chain fatty acids and more gases such as hydrogen and carbon dioxide are formed.

  too little — If little fibre arrives, fewer short-chain fatty acids are formed; in animal models bacteria then turn more to the sugar chains of the mucus.

  observed in studies · Source 3, 4

• Akkermansia — A. muciniphila Akkermansia muciniphila lives in the mucus layer and feeds on its sugar chains. For this it has a large number of its own enzymes. This produces acetate and propionate for its neighbours. Source 4↕ both, depending on amount Akkermansia feeds on the mucus by breaking down its sugar chains, and in doing so supplies acetate and propionate to its neighbours. In animal models the gut wall then makes more new mucus. observed in studies Source 4
  ⚖ When the balance tips

  too much — If mucus-degrading bacteria break down more than the goblet cells replace, the mucus layer becomes thinner; in animal models this happens mainly when little fibre arrives.

  too little — If little Akkermansia is present, the sugar chains of the mucus are broken down more slowly, and butyrate producers in the mucus layer receive fewer breakdown products. This has been shown in mixed cultures.

  observed in studies · Source 4, 8

• Mucus (mucin) — Layer over the gut wall Goblet cells release mucins, large proteins with many sugar chains. They form the sliding layer between the gut contents and the gut wall. The mucus also keeps bacteria away from the gut wall. Source 4↑ supplies The mucus keeps bacteria at a distance from the gut wall and at the same time supplies sugar chains as food for species that live in it. established physiology Source 4
  ⚖ When the balance tips

  too much — If a lot of mucin is released, the layer over the gut wall is thicker, and mucus degraders such as Akkermansia have more food.

  too little — If little mucin is replaced or more of it is broken down, the layer becomes thinner, and bacteria come closer to the gut wall. This is described mainly in animal models.

  observed in studies · Source 4

• Enterococcus faecalis — lactic acid bacterium Enterococcus faecalis lives in small numbers in the gut. It grows with and without oxygen, tolerates bile and salt and ferments sugars almost entirely to lactic acid (lactate). It is naturally insensitive to cephalosporins. Source 11↕ both, depending on amount It supplies lactate to fermentation. At the same time it releases superoxide to the outside via a quinone in its cell membrane; in animal models, hydrogen peroxide in stool rises with its colonisation. Which side dominates depends on numbers and surroundings. observed in studies Source 11, 12
  ⚖ When the balance tips

  too much — If competing bacteria are missing, for instance after antibiotics to which enterococci are insensitive, they can multiply strongly; in animal models, enterococci then displaced a large part of the remaining gut flora.

  too little — If few enterococci are present, lactate formation is carried out by other lactic acid bacteria such as lactobacilli; no task of their own that would then go unfulfilled has been described.

  observed in studies · Source 13, 11

Cofactors in this pathway

• Thiamine (vitamin B1) — As thiamine diphosphate, cofactor of phosphoketolase in the bifid shunt of bifidobacteria; without TPP the shunt stalls Source 6
• Riboflavin (vitamin B2) — As FAD, part of the enzyme pair butyryl-CoA dehydrogenase and EtfAB in butyrate formation; this forms butyryl-CoA Source 7
• Niacin (NAD⁺) — NADH supplies the electrons for the reduction steps in butyrate formation; NADH is turned into NAD⁺ Source 5, 7
• Iron — Iron-sulphur centres in ferredoxin, which accepts electrons during butyrate formation; this yields energy Source 7
• Pantothenic acid (coenzyme A) — Building block of coenzyme A, which butyryl-CoA:acetate CoA-transferase acts on; butyryl-CoA thus becomes butyrate Source 1, 5
• Vitamin B12 (cobamides) — Pseudo-B12 formed by Eubacterium hallii allows Akkermansia to form propionate; succinate thus becomes propionate Source 8

Sources

1. Louis P, Flint HJ. Formation of propionate and butyrate by the human colonic microbiota. Environ Microbiol 2017 · PubMed 27928878
2. Rivière A, Selak M, Lantin D et al. Bifidobacteria and Butyrate-Producing Colon Bacteria: Importance and Strategies for Their Stimulation in the Human Gut. Front Microbiol 2016 · PubMed 27446020
3. Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F. From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. Cell 2016 · PubMed 27259147
4. Ioannou A, Berkhout MD, Scott WT et al. Akkermansia muciniphila: biology, microbial ecology, host interactions and therapeutic potential. Nat Rev Microbiol 2025 · PubMed 39406893
5. Louis P, Flint HJ. Diversity, metabolism and microbial ecology of butyrate-producing bacteria from the human large intestine. FEMS Microbiol Lett 2009 · PubMed 19222573
6. Suzuki R, Katayama T, Kim BJ et al. Crystal structures of phosphoketolase: thiamine diphosphate-dependent dehydration mechanism. J Biol Chem 2010 · PubMed 20739284
7. Buckel W, Thauer RK. Flavin-Based Electron Bifurcation, A New Mechanism of Biological Energy Coupling. Chem Rev 2018 · PubMed 29561602
8. Belzer C, Chia LW, Aalvink S et al. Microbial Metabolic Networks at the Mucus Layer Lead to Diet-Independent Butyrate and Vitamin B12 Production by Intestinal Symbionts. mBio 2017 · PubMed 28928206
9. Zmora N, Zilberman-Schapira G, Suez J et al. Personalized Gut Mucosal Colonization Resistance to Empiric Probiotics Is Associated with Unique Host and Microbiome Features. Cell 2018 · PubMed 30193112
10. Hill C, Guarner F, Reid G et al. Expert consensus document. The International Scientific Association for Probiotics and Prebiotics consensus statement on the scope and appropriate use of the term probiotic. Nat Rev Gastroenterol Hepatol 2014 · PubMed 24912386
11. García-Solache M, Rice LB. The Enterococcus: a Model of Adaptability to Its Environment. Clin Microbiol Rev 2019 · PubMed 30700430
12. Huycke MM, Abrams V, Moore DR. Enterococcus faecalis produces extracellular superoxide and hydrogen peroxide that damages colonic epithelial cell DNA. Carcinogenesis 2002 · PubMed 11895869
13. Ubeda C, Taur Y, Jenq RR et al. Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans. J Clin Invest 2010 · PubMed 21099116

Whole pathway: Gut bacteria

Related pathways

• Gut microbiome — dietary fibre

As of 2026-09-16. Draft written by Claude to schema v2; sources checked in PubMed; expert review pending
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