The Gut Microbiota Function | Encyclopedia MDPI

The Gut Microbiota Function: Comparison

Please note this is a comparison between Version 2 by Camila Xu and Version 1 by Guillermo García Pérez de Sevilla.

The microbiota is known as the set of microorganisms residing in each ecosystem, with a symbiotic relationship and with adaptive properties and rapid renewal, forming a large metabolic unit. The intestinal microbiota is a set of microorganisms made up of approximately 100,000 million bacteria that live in peourple intestine. The microbiota is responsible, among other functions, for maintaining the well-being of the intestinal mucosa, helping us digest food and converting harmful elements into less toxic substances.

gut microbiota
exercise
health

1. Gut Microbiota

The main objective of the narrative is to analyze the association between the intestinal microbiota and exercise and to conclude if there is sufficient evidence to consider new approaches for intestinal recovery and protection as a new important factor in performance.

Joshua Lederberg, an American biologist who received the Nobel Prize in Medicine in 1958, stated that the microorganisms found in humans protect uspeople symbiotically in outheir own body. These communities of microorganisms, known today under the term microbiota, consist of a variety of microorganisms that includes eukaryotes, archaea, bacteria, and viruses, constituting about 1.3% of the body mass, and are essential to maintain optimal health. These microorganisms inhabit different parts of the body, colonizing the mucosa within a given anatomical niche, such as the respiratory system, the walls of the digestive system or also the urogenital system, among other surfaces ^[1]. More diversity of the microbiota is found in the intestinal tract and mouth, while the skin contains less diversity, followed by the vagina, although a consensus has not yet been reached on the number of species that inhabit it ^[2].

In 2014, the term “intestinal flora” was coined to describe the intestinal microbiota, although later, it was changed to gut microbiota ^[3].

Some gut microbiota bacteria attach to the cells’ external wall and to specific receptors called adhesins. They can adapt to the specific conditions of the environment, such as humidity, temperature, or pH, being able to activate defense mechanisms in case of interaction, for example, with a harmful virus. The homeostasis of the intestinal tract depends on the balance between the microbiota, intestinal permeability, and local immunity; in the event of any non-adaptive alteration, it can produce negative effects on the host itself. When these alterations occur, it is known as intestinal dysbiosis, which can affect digestion, nutrient absorption, vitamin production, and the control of harmful microorganisms ^[3].

Most of the bacteria that make up the gut microbiota live in the colon ^[4]. The colon is described as a potentially active organ due to the extensive activity of the gut microbiota and has been compared to the liver due to its high metabolic capacity ^[5]. The microbiota is dominated by four main phyla: Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria ^[6]. Although there are also bacteria in smaller proportions that are vital for the function of the microbiota, Firmicutes and Bacteriodetes stand out due to their proportion throughout the intestinal tract, as they represent 60% and 20%, respectively, of all the gut microbiota, while the Proteobacteria phylum covers 5% and Actinobacteria 3%, approximately ^[7].

2. The Gut Microbiota Function

The functions of the gut microbiota include the following:

2.1. Protection Function in the Intestinal Barrier

The gut microbiota plays an important role in helping to maintain the integrity of the intestinal barrier, thus protecting the host from pathogens. In turn, the microbiota develops defense mechanisms together with the epithelial cells, which are responsible for establishing an effective and harmonious intestinal barrier, preventing the passage of harmful substances, antigens, toxins, and microbial products and, on the other hand, the absorption of nutrients benign ^[8].

The main elements that form the intestinal barrier are the mucus, the tight junctions between enterocytes, antimicrobial peptides, and immunoglobulin A (IgA) secretion ^[9]. The intercellular junctions of the intestinal barrier separate the internal environment from the external environment, making it impermeable to certain pathogenic substances and permeable to nutrients ^[10].

The mucosa interacts with the microbiota to maintain intestinal homeostasis; in addition, the intestinal microbiota induces the biosynthesis of antimicrobial peptides by mucosal Paneth cells, such as cathelicidins, lectins, and defensins, by activating their membrane receptors. Bacteriodetes thetaiotaomicron and Lactobacillus innocua are two of the main agents that stimulate Paneth cells ^[11].

Another reinforcement of this barrier function by the microbiota of the intestinal lumen is the production of lactic acid by Lactobacillus, which reinforces the ability of human lysozyme released in the lumen to destroy peptidoglycan ^[12]. Short-chain fatty acids (SCFAs) released by bacterial fermentation also stimulate the production of the antimicrobial peptide cathelicidin. These SCFAs acidify the intestinal lumen and prevent colonization by pathogens sensitive to this pH, such as Salmonella, Escherichia, and Clostridium difficile ^[9].

The homeostasis of the barrier function would result in an optimal symbiosis; otherwise, if the function of the intestinal barrier does not favor an adequate mechanism, it will have an exaggerated or abnormal immune response that would lead to poor control of intestinal permeability, leading to what weis knowing as intestinal dysbiosis [13,14]^[13][14].

2.2. Function on the Development of the Immune System

The gut microbiota contributes to gut immunomodulation in conjunction with the innate and adaptive immune systems ^[9]. In line with the previous protection function, the immune system has co-evolved to maintain a symbiotic relationship with the commensal species of the microbiota while keeping other species considered pathogenic in this intestinal ecosystem under control. About 70% of the lymphocytes in the human body live in the digestive system, which gives us an idea of the importance of this function in the development ^[15].

Components and cell types of the immune system involved in the immunomodulatory process include gut-associated lymphoid tissues (GALT), effector and regulatory T cells, IgA-producing B (plasma) cells, Group 3 innate lymphoid cells, resident macrophages, and dendritic cells in the lamina itself ^[16].

The role of the gut microbiota in forming a functional GALT is implicit in the poor development of Peyer’s patches and isolated lymphoid follicles that are marked by an abundance of IgE B cells rather than IgA B cells ^[17]. The absence of the intestinal microbiota causes the plasma cell populations of the intestinal mucosa to differentiate mainly towards greater production of IgE, instead of IgA, which is associated with an increased risk of allergies ^[14].

Effector T cells are regulated in the mucosa by Th17 cells. Some bacteria, such as Bacillus fragilis, belonging to the Bifidobacterium or Clostridium genera, activate Treg lymphocytes via Toll-like receptors (TLR) that are part of the innate immune system, inducing systemic anti-inflammatory effects, which helps to develop tolerance to antigens present in the diet and some bacteria in the lumen ^[16].

This cross-communication between the microbiota and the epithelial cells is also responsible for the release of IgA and for stimulating the production of glycoproteins to form more mucus. The main stimulators of epithelial IgA production are Gram-negative species such as Bacteroides, which activate dendritic cells in the mucosa so that they induce IgA production by plasma cells (activated lymphocytes) in the submucosa. This IgA prevents microorganisms from activating pro-inflammatory pathways, as they cannot bind when coated by these antibodies, to receptors such as TLRs. In turn, IgA collaborates in capturing antigens and prevents their penetration through the intestinal barrier, limiting the movement of pathogens and neutralizing toxins throughout the lumen ^[18]. The presence of high populations of Suturella, on the other hand, reduces IgA production in the lumen, since this bacterium releases IgA-degrading proteases ^[15]. The complexity of the intestinal microbiota, per se, is a defense against the colonization of this ecosystem by other types of microorganisms ^[18]. This is especially important in adults who have a much more stable intestinal microbiota than children or subjects with intestinal dysbiosis. The production of bacteriocins by the resistant microbiota is responsible for this resistance to colonization of the lumen by other bacteria. Similarly, the bacteriophages in the intestinal lumen can prevent the establishment of susceptible bacterial species. All these mechanisms prevent the bacterial translocation factor through the intestinal epithelium and therefore prevent a systemic immune response to a possible infection ^[19].

2.3. The Intestinal Microbiota Performs a Metabolic Function

Contributing to the digestion of nutrients from the diet ^[9]. The gut microbiota obtains its nutrients mainly from carbohydrates in the diet. Fermentation of carbohydrates that escape proximal digestion and indigestible oligosaccharides are metabolized by bacteria such as Bacteroides, Roseburia, Bifidobacterium, Faecalibacterium, and Enterobacteria, resulting in the synthesis of SCFAs such as butyrate, propionate, and acetate, which are rich sources of energy for the host ^[20].

This metabolic process is favored by the more acidic pH of the right colon. In contrast, in the left colon, microorganisms grow more slowly due to the low arrival of food with a more neutral pH ^[21].

Members of the genus Bacteroides are the predominant organisms involved in carbohydrate metabolism, achieved by expressing enzymes such as glycosyltransferases, glycoside hydrolases, and polysaccharide lyases. The best example among these organisms is Bacteroides thetaiotaomicron, which is endowed with a genome encoding more than 260 hydrolases ^[22].

The gut microbiota also has an efficient protein metabolizing machinery that functions through microbial proteinases and peptidases in conjunction with human proteinases. Various amino acid transporters in the bacterial cell wall facilitate the entry of amino acids from the intestinal lumen into the bacteria, where they convert the amino acids into small signaling molecules and antimicrobial peptides (bacteriocins) ^[23].

Another metabolic function of great importance is described in the literature, such as the synthesis of vitamins such as vitamin K and vitamin B, and the function of lipid regulation. In addition, members of the genus Bacteroides synthesize conjugated linoleic acid (CLA), which has antidiabetic, antiatherogenic, antiobesogenic, hypolipidemic, and immunomodulatory properties ^[24]. The gut microbiota has also been shown to positively impact lipid metabolism by suppressing the inhibition of lipoprotein lipase (LPL) activity in adipocytes ^[25].

References

Brüls, T.; Weissenbach, J. The human metagenome: Our other genome? Hum. Mol. Genet. 2011, 20, 142–148.
Prats, G. Microbiologia y Parasitología Médica; Médica Panamericana: Madrid, Spain, 2012; ISBN 9788498354294.
Sebastián-Domingo, J.J.; Sánchez-Sánchez, C. From the intestinal flora to the microbiome. Rev. Esp. Enferm. Dig. 2018, 110, 51–56.
Richmond, C.R. ICRP report of the task group on reference man. Int. J. Nucl. Med. Biol. 1985, 12, 251.
Hopkins, M.J.; Macfarlane, G.T.; Furrie, E.; Fite, A.; Macfarlane, S. Characterisation of intestinal bacteria in infant stools using real-time PCR and northern hybridisation analyses. FEMS Microbiol. Ecol. 2005, 54, 77–85.
Stephens, R.W.; Arhire, L.; Covasa, M. Gut Microbiota: From Microorganisms to Metabolic Organ Influencing Obesity. Obesity 2018, 26, 801–809.
Sun, J.; Kato, I. Gut microbiota, inflammation and colorectal cancer. Genes Dis. 2016, 3, 130–143.
Rowland, I.; Gibson, G.; Heinken, A.; Scott, K.; Swann, J.; Thiele, I.; Tuohy, K. Gut microbiota functions: Metabolism of nutrients and other food components. Eur. J. Nutr. 2018, 57, 1–24.
Jandhyala, S.M. Role of the normal gut microbiota. World J. Gastroenterol. 2015, 21, 8787.
Rakoff-Nahoum, S.; Paglino, J.; Eslami-Varzaneh, F.; Edberg, S.; Medzhitov, R. Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis. Cell 2004, 118, 229–241.
Kim, D.; Yoo, S.A.; Kim, W.U. Gut microbiota in autoimmunity: Potential for clinical applications. Arch. Pharm. Res. 2016, 39, 1565–1576.
Ren, C.; Dokter-Fokkens, J.; Figueroa Lozano, S.; Zhang, Q.; de Haan, B.J.; Zhang, H.; Faas, M.M.; de Vos, P. Lactic Acid Bacteria May Impact Intestinal Barrier Function by Modulating Goblet Cells. Mol. Nutr. Food Res. 2018, 62, 1700572.
Turner, J.R. Intestinal mucosal barrier function in health and disease. Nat. Rev. Immunol. 2009, 9, 799–809.
Vancamelbeke, M.; Vermeire, S. The intestinal barrier: A fundamental role in health and disease. Expert Rev. Gastroenterol. Hepatol. 2017, 11, 821–834.
Kim, D.; Zeng, M.Y.; Núñez, G. The interplay between host immune cells and gut microbiota in chronic inflammatory diseases. Exp. Mol. Med. 2017, 49, e339.
Honda, K.; Littman, D.R. The microbiota in adaptive immune homeostasis and disease. Nature 2016, 535, 75–84.
Durkin, H.G.; Bazin, H.; Waksman, B.H. Origin and fate of IgE-bearing lymphocytes: I. Peyer’s patches as differentiation site of cells simultaneously bearing IgA and IgE. J. Exp. Med. 1981, 154, 640–648.
Cani, P.D.; Van Hul, M.; Lefort, C.; Depommier, C.; Rastelli, M.; Everard, A. Microbial regulation of organismal energy homeostasis. Nat. Metab. 2019, 1, 34–46.
Theilmann, M.C.; Goh, Y.J.; Nielsen, K.F.; Klaenhammer, T.R.; Barrangou, R.; Hachem, M.A. Lactobacillus acidophilus metabolizes dietary plant glucosides and externalizes their bioactive phytochemicals. MBio 2017, 8, e01421-17.
Macfarlane, G.T.; Cummings, J.H.; Allison, C. Protein degradation by human intestinal bacteria. J. Gen. Microbiol. 1986, 132, 1647–1656.
Morales, P.; Brignardello, J.; Gotteland, M. La microbiota intestinal: Un nuevo actor en el desarrollo de la obesidad. Rev. Med. Chile 2010, 138, 1020–1027.
Cantarel, B.L.; Lombard, V.; Henrissat, B. Complex carbohydrate utilization by the healthy human microbiome. PLoS ONE 2012, 7, e28742.
De Biase, D.; Pennacchietti, E. Glutamate decarboxylase-dependent acid resistance in orally acquired bacteria: Function, distribution and biomedical implications of the gadBC operon. Mol. Microbiol. 2012, 86, 770–786.
Churruca, I.; Fernández-Quintela, A.; Portillo, M.P. Conjugated linoleic acid isomers: Differences in metabolism and biological effects. BioFactors 2009, 35, 105–111.
Devillard, E.; McIntosh, F.M.; Duncan, S.H.; Wallace, R.J. Metabolism of linoleic acid by human gut bacteria: Different routes for biosynthesis of conjugated linoleic acid. J. Bacteriol. 2007, 189, 2566–2570.