Dysbiosis

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Dysbiosis (also called dysbacteriosis) is characterized as a disruption to the microbiota homeostasis caused by an imbalance in the microflora, changes in their functional composition and metabolic activities, or a shift in their local distribution. It is a term for a microbial imbalance or maladaptation on or inside the body,[1][2] such as an impaired microbiota. For example, a part of the human microbiota, such as the skin flora, gut flora, or vaginal flora, can become deranged, with normally dominating species underrepresented and normally outcompeted or contained species increasing to fill the void. Dysbiosis is most commonly reported as a condition in the gastrointestinal tract,[2] particularly during small intestinal bacterial overgrowth (SIBO) or small intestinal fungal overgrowth (SIFO).[3][4]

Typical microbial colonies found on or in the body are normally benign or beneficial. These beneficial and appropriately sized microbial colonies carry out a series of helpful and necessary functions, such as aiding in digestion.[5] They also help protect the body from the penetration of pathogenic microbes. These beneficial microbial colonies compete with each other for space and resources.[6]

Causes[edit]

Dysbiosis may be caused by such diverse things as antibiotic or mold exposure,[7][8][unreliable medical source?] alcohol misuse,[9][10] or inappropriate diet.[11][unreliable medical source?] Many of these things can lead to interruptions in the human body like the oral cavity[12] and gut flora[13] which has been linked to a variety of diseases such as IBD, ulcerative colitis, allergies and more.[13]

Gut[edit]

Bacteria in the human gut’s intestines are the most diverse in the human body and play a vital role in human health. The consumer’s dietary habits can be one of the most influential factors on the gut’s microbiota.[14] Diets high in carbohydrates and refined sugars are common links to dysbiosis in the gut, whereas foods rich in fruits, vegetables, and fish oils are considered more favorable to the gut due to their anti-inflammatory properties.[13] Many diseases, such as IBD, Type 2 Diabetes, Crohn's, and even allergies, are suggested to be due, in part, to an alteration in the microbiome of the gut.[13][14]

Oral[edit]

Dysbiosis can be sectioned into different compartments of the human body. The oral cavity is no exception. What enters the mouth is one of the first exposures to microbes involved in this process and can also lead to other microbial disturbances such as in the gut and intestines.[15] Hygiene and nutritional variation are imperative in preventing oral diseases such as gingivitis, tooth decay, cavities, etc., which are linked to the interrupted microbial community in the oral cavity.[12] Oral pathogens can trigger dysbiotic functions throughout multiple microbiota compartments of the body and alter systemic processes, such as immunological or digestion interruptions. Smoking, drinking, oral intercourse, salivary glands, and age are all considered links to sources that can lead to oral dysbiosis.[12]

Antibiotics[edit]

Dysbiosis can occur during many stages of life and can be triggered by many different sources, antibiotics, for example, being a significant contributor to disruptions in microbiotas. Antibiotic usage during young childhood development can lead to adverse gut issues (dysbiosis) in adulthood.[16] The gut microbiome is altered from antibiotics and is linked to future gut disease, i.e., IBD, ulcerative colitis, obesity, etc. The intestinal immune system is directly influenced by the gut microbiome and can be hard to recover if damaged through antibiotics.[16]

Effects[edit]

Gut dysbiosis has been linked to the “pathogenesis of both intestinal and extra-intestinal disorders."[14] Intestinal disorders include IBD, IBS, and coeliac disease, and extra-intestinal conditions have allergies, asthma, metabolic syndrome, cardiovascular disease, and obesity.[14] Dysbiosis has played a role in autoimmune diseases, allergies, and metabolic disorders.

Gut dysbiosis can also be a factor in neurodegenerative and cerebrovascular diseases due to the link between age-related dysbiosis and neurological decline by inflammation being the common factor for a wide variety of age-related pathologies.[17] By correcting the dysbiosis in elderly patients, it may be possible to prevent the development of neurodegenerative diseases.[18] Dysbiosis may contribute to the cause or development of neurological conditions, including “autism, pain, depression, anxiety, and stroke.”[19] Dysbiosis contributing to neurological conditions is due to interactions with the gut-brain axis allowing the gut microbiome to influence neural development, cognition, and behavior.[17] There has also been evidence that the gut microbiota composition can be altered due to changes in behavior, and changing the microbiome can also cause depressive-like behaviors.[17]

When this balance is disturbed, these colonies exhibit a decreased ability to check each other's growth, which can then lead to overgrowth of one or more of the disturbed colonies which may further damage some of the other smaller beneficial ones in a vicious cycle. As more beneficial colonies are damaged, making the imbalance more pronounced, more overgrowth issues occur because the damaged colonies are less able to check the growth of the overgrowing ones. If this goes unchecked long enough, a pervasive and chronic imbalance between colonies will set in, which ultimately minimizes the beneficial nature of these colonies as a whole.

Microbial colonies also excrete many different types of waste byproducts.[14] Using different waste removal mechanisms, under normal circumstances the body effectively manages these byproducts with little or no trouble. Unfortunately, oversized and inappropriately large colonies, due to their increased numbers, excrete increased amounts of these byproducts. As the amount of microbial byproducts increases, the higher waste byproducts levels can overburden the body's waste removal mechanisms.

It is the combination of these two negative outcomes that causes many of the negative health symptoms observed when dysbiosis is present.

A human’s microbiome can change because of inflammatory processes, such as cell-mediated inflammation and host-mediated inflammation, or a ‘driver’ bacteria causing/aggravating inflammation. This change allows the microbial community to become more susceptible to pathogens. Once the pathogens are established successfully, they contribute to dysbiosis and produce genotoxins and other potential cancer-causing microbial metabolites.[20] The evolution of pathogens is another possible effect of dysbiosis, contributing to a potential increase in cancer risk.[20]

Gut dysbiosis can affect the cardiovascular system “via signaling molecules and bioactive metabolites.[18] This could cause diseases through neuro-entero-endocrine hormones that can lead to heart failure and other conditions such as chronic kidney disease, hypertension, obesity, and diabetes.[18]

Associated illnesses[edit]

Cross-regulation occurs between the host and the gut microbiota in healthy people, resulting in a homeostatic equilibrium of bacteria that keeps the gastrointestinal tract healthy and free of potentially pathogenic bacteria.[21] There are three significant categories of dysbiosis: loss of beneficial organisms, excessive growth of potentially harmful microorganisms, and loss of overall microbial diversity.[21] Disruptions in the microbiome can allow outside factors or even pathogenic members of the microbiome to take hold in the gut environment. Dysbiosis has been reported to be associated with illnesses, such as multiple chemical sensitivity, periodontal disease,[22] inflammatory bowel disease,[23][24] chronic fatigue syndrome,[25] obesity,[26][27] cancer,[28][29] bacterial vaginosis,[30] and colitis.[31]

IBD[edit]

There is no mono-associated cause of IBD; the three major pathogens that have been associated with IBD are Mycobacterium avium paratuberculosis (MAP), adherent-invasive escherichia coli (AICE), and clostridium difficile.[21] There is no evidence that these pathogens are the culprit of IBD. Rather than the “one-microbe-one disease” hypothesis, it is thought that IBD is caused by an imbalance of commensal microflora associated with more complex interactions between the host and the entire intestinal microbiota.[21]

Obesity[edit]

Obesity is a metabolic condition in which the body retains an unhealthy amount of fat.[21] The prevalence of obesity in the United States is increasing, with about 93.3 million adults and 14.4 million children recorded in 2015-2016, according to the Center for Disease Control and Prevention. Similar to IBD, a specific microbiota appears to be linked to the development of obesity. There is a notable reduction in microbial diversity in obese individuals. Research in humans and animals shows an association of obesity with altered ratios between Bacteroidetes and Firmicutes; as Bacteriodetes decreases, Firmicutes increases.[21] This ratio has been linked to body weight and fat accumulation, indicating that obese people have a higher disproportionate ratio of these bacteria.[21]

Diabetes Mellitus[edit]

Diabetes mellitus (DM) is a carbohydrate metabolism disorder characterized by insufficient insulin output or utilization, which is needed for the body to turn sugars and starches into energy. The prevalence of DM in the United States is about 29.1 million, with about 1.7 million new diagnoses annually.[21] The two forms of diabetes are Type 1 and Type 2. Type 1 DM is also known as Insulin-Dependent Diabetes Mellitus (IDDM). Type 1 diabetes is an autoimmune condition that affects the beta cells in the pancreas, causing insulin production to be impaired.[21] It is most often diagnosed in children and young adults. Type 2 diabetes mellitus, also known as Non-Insulin-Dependent Diabetes Mellitus (NIDDM), is a type of diabetes that affects adults and is characterized by insulin resistance, which occurs when tissue sensitivity insulin is reduced, causing the body to ignore the insulin released. Research has shown dysbiosis of the intestinal microbiota may contribute to both forms of diabetes. Dysbiosis related to type 1 DM is characterized by a decline in mucin-degrading bacteria, such as Bifidobacteria, Lactobacillus, and Prevotella, and an increase in Bacteroidetes and Clostridium.[21]

Cancer[edit]

Sustained periods of dysbiosis lead to extended amounts of stress and inflammation in the gut microbiome, which can in turn promote the production of carcinogenic metabolites.[20] Intestinal dysbiosis has been associated with colorectal cancer (CRC). According to the American Cancer Society, colorectal cancer is the third most common cancer and the second leading cause of cancer death in the United States.[21] In CRC patients, a general dysbiosis pattern has been discovered, including a decrease in butyrate-producing bacteria and an increase in the proportion of several potentially pathogenic bacteria.[21]

Clostridioides difficile[edit]

C. difficile is an opportunistic bacteria that commonly infects patients following a disruption in the microbiome, such as treatment with antibiotics.[32][33] Infection can lead to several different symptoms including watery diarrhea, fever, loss of appetite, nausea, and abdominal pain.[34] Severe or chronic infections of C. difficile can lead to inflammation of the colon, a condition known as colitis.[35]

Periodontitis[edit]

Periodontitis is an oral infection that can damage the bones supporting teeth and lead to tooth loss.[36] One of the major risk factors for periodontitis is the disruption of the oral microbiome such that there is an accumulation of pathogenic bacteria.[22] Studies show that the oral microbiota changes as periodontitis progress, shifting from gram-positive aerobes to gram-negative anaerobes. Oral dysbiosis is likely to evolve, shifting the symbiotic host-microbe relationship to a pathogenic one. During this time, the host's oral health deteriorates, eventually leading to clinical disease.[22]

Treatments[edit]

Antibiotics[edit]

Because of the complex interactions in the microbiome, not much data exists on the efficacy of using antibiotics to treat dysbiosis. However, a broad-spectrum antibiotic that has low impact on the intestinal gut microbiome called rifaximin, has been shown to be effective in improving several of the ailments associated with dysbiosis, including irritable bowel syndrome,[37] ulcerative colitis[38] and Crohn's disease.[39]

While most antibiotics alter the gut microbiota for the duration of the treatment, some cause long-lasting changes. However, repeated exposure to antibiotics can also cause the opposite of the intended effect and destabilize the gut microbiome, resulting in promoting “outgrowth of antibiotic-resistant pathogenic bacteria.”[40]

Fecal microbiota transplant (FMT)[edit]

Fecal Microbiota Transplantation (FMT) is an experimental treatment that has resolved 80-90 percent of dysbiosis-related infections caused by recurrent C. difficile infections that do not respond to antibiotics in randomized, controlled clinical trials.[41] A patient's colon is transplanted during FMT with a fecal preparation from a carefully screened, healthy stool donor. FMT is thought to work by repopulating the patient's microbiome with various microorganisms that compete with C. difficile for space.[42]

FMTs use the same line of reasoning as probiotics; to recreate a healthy balance of microbiota in the microbiome by inserting beneficial microbes into the environment. FMT accomplishes this by taking a donation of fecal matter from a healthy individual, diluted, strained and introduced to a diseased patient.[43] FMTs are currently used to treat patients with Clostridium difficile infections, who have proved resistant to other therapies.;[44] however, this is considered an investigational therapy at present with risks that have not been fully defined.[45] Because the process is not sterile and contaminations can pass from donor to patient, there is a push to isolate key microbiota and culture them independently.[46]

Probiotics[edit]

The World Health Organization defines probiotics as "live microorganisms, which when administered in adequate amounts, confer a health benefit on the host".[47] The benefit of using probiotics to treat dysbiosis related diseases lies in its ability to treat the underlying cause of said diseases. Some benefits include their ability to suppress inflammation in the microbiome[48][49] and disrupt colonization by pathogens.[50]

Excessive use of antibiotics, IBD, obesity, diabetes, cardiovascular disease, and many more ailments are related to interruptions in the microbiome(dysbiosis), especially in the human gut. Probiotics can promote healthier microbial function by introducing or reintroducing helpful bacteria to strengthen the weaknesses presented in a dysbiotic microbiome.[51] It is essential to recognize that such circumstances are beneficial bacteria that occur more frequently than harmful ones. Probiotics can be utilized in aiding existing conditions and preventing such diseases by instituting antiinflammatory properties and improving immune cell function.[51]

The human gut contains a wide diversity of bacteria and can easily be disrupted through diet, medicinal usage, diseases, and many others. Probiotics have proven influential in returning the intestinal microbiota to homeostatic balance and improve intestinal health.[52] Probiotics contain anti-inflammatory properties that assist in the prevention and treatment of intestinal diseases due to microbial dysbiosis. More research is needed to understand better the many benefits probiotics can offer for multiple forms of dysbiosis.[52]

See also[edit]

Notes and references[edit]

  1. ^ Tamboli CP, Neut C, Desreumaux P, Colombel JF (January 2004). "Dysbiosis in inflammatory bowel disease". Gut. 53 (1): 1–4. doi:10.1136/gut.53.1.1. PMC 1773911. PMID 14684564.
  2. ^ a b Moos WH, Faller DV, Harpp DN, Kanara I, Pernokas J, Powers WR, Steliou K (2016). "Microbiota and Neurological Disorders: A Gut Feeling". BioResearch Open Access. 5 (1): 137–45. doi:10.1089/biores.2016.0010. PMC 4892191. PMID 27274912. As reviewed in this report, synthetic biology shows potential in developing microorganisms for correcting pathogenic dysbiosis (gut microbiota-host maladaptation), although this has yet to be proven.
  3. ^ Fujimori S (June 2015). "What are the effects of proton pump inhibitors on the small intestine?". World Journal of Gastroenterology. 21 (22): 6817–9. doi:10.3748/wjg.v21.i22.6817. PMC 4462721. PMID 26078557. Several meta-analyses and systematic reviews have reported that patients treated with PPIs, as well as post-gastrectomy patients, have a higher frequency of small intestinal bacterial overgrowth (SIBO) compared to patients who lack the aforementioned conditions. Furthermore, there is insufficient evidence that these conditions induce Clostridium difficile infection. At this time, PPI-induced dysbiosis is considered a type of SIBO.
  4. ^ Erdogan A, Rao SS (April 2015). "Small intestinal fungal overgrowth". Current Gastroenterology Reports. 17 (4): 16. doi:10.1007/s11894-015-0436-2. PMID 25786900. Small intestinal fungal overgrowth (SIFO) is characterized by the presence of excessive number of fungal organisms in the small intestine associated with gastrointestinal (GI) symptoms. Candidiasis is known to cause GI symptoms particularly in immunocompromised patients or those receiving steroids or antibiotics. However, only recently, there is emerging literature that an overgrowth of fungus in the small intestine of non-immunocompromised subjects may cause unexplained GI symptoms. Two recent studies showed that 26 % (24/94) and 25.3 % (38/150) of a series of patients with unexplained GI symptoms had SIFO. The most common symptoms observed in these patients were belching, bloating, indigestion, nausea, diarrhea, and gas. The underlying mechanism(s) that predisposes to SIFO is unclear but small intestinal dysmotility and use of proton pump inhibitors has been implicated. However, further studies are needed; both to confirm these observations and to examine the clinical relevance of fungal overgrowth, both in healthy subjects and in patients with otherwise unexplained GI symptoms.
  5. ^ Kau AL, Ahern PP, Griffin NW, Goodman AL, Gordon JI (June 2011). "Human nutrition, the gut microbiome and the immune system". Nature. 474 (7351): 327–36. doi:10.1038/nature10213. PMC 3298082. PMID 21677749.
  6. ^ Xuan C, Shamonki JM, Chung A, Dinome ML, Chung M, Sieling PA, Lee DJ (2014-01-08). "Microbial dysbiosis is associated with human breast cancer". PLOS ONE. 9 (1): e83744. Bibcode:2014PLoSO...983744X. doi:10.1371/journal.pone.0083744. PMC 3885448. PMID 24421902.
  7. ^ Mikkelsen KH, Allin KH, Knop FK (May 2016). "Effect of antibiotics on gut microbiota, glucose metabolism and body weight regulation: a review of the literature". Diabetes, Obesity & Metabolism. 18 (5): 444–53. doi:10.1111/dom.12637. PMID 26818734.
  8. ^ Hawrelak JA, Myers SP (June 2004). "The causes of intestinal dysbiosis: a review" (PDF). Alternative Medicine Review. 9 (2): 180–97. PMID 15253677. Archived from the original (PDF) on 2011-07-17.
  9. ^ Yan AW, Fouts DE, Brandl J, Stärkel P, Torralba M, Schott E, et al. (January 2011). "Enteric dysbiosis associated with a mouse model of alcoholic liver disease". Hepatology. 53 (1): 96–105. doi:10.1002/hep.24018. PMC 3059122. PMID 21254165.
  10. ^ Mutlu E, Keshavarzian A, Engen P, Forsyth CB, Sikaroodi M, Gillevet P (October 2009). "Intestinal dysbiosis: a possible mechanism of alcohol-induced endotoxemia and alcoholic steatohepatitis in rats". Alcoholism, Clinical and Experimental Research. 33 (10): 1836–46. doi:10.1111/j.1530-0277.2009.01022.x. PMC 3684271. PMID 19645728.
  11. ^ Chan YK, Estaki M, Gibson DL (2013). "Clinical consequences of diet-induced dysbiosis". Annals of Nutrition & Metabolism. 63 Suppl 2 (suppl2): 28–40. doi:10.1159/000354902. PMID 24217034.
  12. ^ a b c Chimenos-Küstner E, Giovannoni ML, Schemel-Suárez M (October 2017). "Dysbiosis as a determinant factor of systemic and oral pathology: importance of microbiome". Medicina Clinica. 149 (7): 305–309. doi:10.1016/j.medcli.2017.05.036. hdl:2445/116548. PMID 28669517.
  13. ^ a b c d Tomasello G, Mazzola M, Leone A, Sinagra E, Zummo G, Farina F, et al. (December 2016). "Nutrition, oxidative stress and intestinal dysbiosis: Influence of diet on gut microbiota in inflammatory bowel diseases". Biomedical Papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia. 160 (4): 461–466. doi:10.5507/bp.2016.052. PMID 27812084.
  14. ^ a b c d e Carding S, Verbeke K, Vipond DT, Corfe BM, Owen LJ (February 2015). "Dysbiosis of the gut microbiota in disease". Microbial Ecology in Health and Disease. 26: 26191. doi:10.3402/mehd.v26.26191. PMC 4315779. PMID 25651997.
  15. ^ Koliarakis I, Messaritakis I, Nikolouzakis TK, Hamilos G, Souglakos J, Tsiaoussis J (August 2019). "Oral Bacteria and Intestinal Dysbiosis in Colorectal Cancer". International Journal of Molecular Sciences. 20 (17): 4146. doi:10.3390/ijms20174146. PMC 6747549. PMID 31450675.
  16. ^ a b Vangay P, Ward T, Gerber JS, Knights D (May 2015). "Antibiotics, pediatric dysbiosis, and disease". Cell Host & Microbe. 17 (5): 553–64. doi:10.1016/j.chom.2015.04.006. PMC 5555213. PMID 25974298.
  17. ^ a b c Rogers GB, Keating DJ, Young RL, Wong ML, Licinio J, Wesselingh S (June 2016). "From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways". Molecular Psychiatry. 21 (6): 738–48. doi:10.1038/mp.2016.50. PMC 4879184. PMID 27090305.
  18. ^ a b c Koszewicz M, Jaroch J, Brzecka A, Ejma M, Budrewicz S, Mikhaleva LM, et al. (February 2021). "Dysbiosis is one of the risk factor for stroke and cognitive impairment and potential target for treatment". Pharmacological Research. 164: 105277. doi:10.1016/j.phrs.2020.105277. PMID 33166735.
  19. ^ Kigerl KA, Hall JC, Wang L, Mo X, Yu Z, Popovich PG (November 2016). "Gut dysbiosis impairs recovery after spinal cord injury". The Journal of Experimental Medicine. 213 (12): 2603–2620. doi:10.1084/jem.20151345. PMC 5110012. PMID 27810921.
  20. ^ a b c Sheflin AM, Whitney AK, Weir TL (October 2014). "Cancer-promoting effects of microbial dysbiosis". Current Oncology Reports. 16 (10): 406. doi:10.1007/s11912-014-0406-0. PMC 4180221. PMID 25123079.
  21. ^ a b c d e f g h i j k l DeGruttola AK, Low D, Mizoguchi A, Mizoguchi E (May 2016). "Current Understanding of Dysbiosis in Disease in Human and Animal Models". Inflammatory Bowel Diseases. 22 (5): 1137–50. doi:10.1097/MIB.0000000000000750. PMC 4838534. PMID 27070911.
  22. ^ a b c Nath SG, Raveendran R (July 2013). "Microbial dysbiosis in periodontitis". Journal of Indian Society of Periodontology. 17 (4): 543–5. doi:10.4103/0972-124X.118334. PMC 3800425. PMID 24174742.
  23. ^ Marteau P (2009). "Bacterial flora in inflammatory bowel disease". Digestive Diseases. 27 Suppl 1: 99–103. doi:10.1159/000268128. PMID 20203504.
  24. ^ Lepage P, Leclerc MC, Joossens M, Mondot S, Blottière HM, Raes J, et al. (January 2013). "A metagenomic insight into our gut's microbiome". Gut. 62 (1): 146–58. doi:10.1136/gutjnl-2011-301805. PMID 22525886.
  25. ^ Lakhan SE, Kirchgessner A (October 2010). "Gut inflammation in chronic fatigue syndrome". Nutrition & Metabolism. 7: 79. doi:10.1186/1743-7075-7-79. PMC 2964729. PMID 20939923.
  26. ^ Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI (December 2006). "An obesity-associated gut microbiome with increased capacity for energy harvest". Nature. 444 (7122): 1027–31. Bibcode:2006Natur.444.1027T. doi:10.1038/nature05414. PMID 17183312.
  27. ^ Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, et al. (January 2009). "A core gut microbiome in obese and lean twins". Nature. 457 (7228): 480–4. Bibcode:2009Natur.457..480T. doi:10.1038/nature07540. PMC 2677729. PMID 19043404.
  28. ^ Castellarin M, Warren RL, Freeman JD, Dreolini L, Krzywinski M, Strauss J, et al. (February 2012). "Fusobacterium nucleatum infection is prevalent in human colorectal carcinoma". Genome Research. 22 (2): 299–306. doi:10.1101/gr.126516.111. PMC 3266037. PMID 22009989.
  29. ^ Kostic AD, Gevers D, Pedamallu CS, Michaud M, Duke F, Earl AM, et al. (February 2012). "Genomic analysis identifies association of Fusobacterium with colorectal carcinoma". Genome Research. 22 (2): 292–8. doi:10.1101/gr.126573.111. PMC 3266036. PMID 22009990.
  30. ^ Africa CW, Nel J, Stemmet M (July 2014). "Anaerobes and bacterial vaginosis in pregnancy: virulence factors contributing to vaginal colonisation". International Journal of Environmental Research and Public Health. 11 (7): 6979–7000. doi:10.3390/ijerph110706979. PMC 4113856. PMID 25014248.
  31. ^ Mazmanian SK (April 2008). "Capsular polysaccharides of symbiotic bacteria modulate immune responses during experimental colitis". Journal of Pediatric Gastroenterology and Nutrition. 46 Suppl 1: E11-2. doi:10.1097/01.mpg.0000313824.70971.a7. PMID 18354314.
  32. ^ Knoop FC, Owens M, Crocker IC (July 1993). "Clostridium difficile: clinical disease and diagnosis". Clinical Microbiology Reviews. 6 (3): 251–65. doi:10.1128/CMR.6.3.251. PMC 358285. PMID 8358706.
  33. ^ Surawicz CM, Brandt LJ, Binion DG, Ananthakrishnan AN, Curry SR, Gilligan PH, et al. (April 2013). "Guidelines for diagnosis, treatment, and prevention of Clostridium difficile infections". The American Journal of Gastroenterology. 108 (4): 478–98, quiz 499. doi:10.1038/ajg.2013.4. PMID 23439232.
  34. ^ "Clostridium difficile Infection Information for Patients". Centers for Disease Control. Retrieved 2018-06-27.
  35. ^ Surawicz CM, McFarland LV, Elmer G, Chinn J (October 1989). "Treatment of recurrent Clostridium difficile colitis with vancomycin and Saccharomyces boulardii". The American Journal of Gastroenterology. 84 (10): 1285–7. PMID 2679049.
  36. ^ "Periodontitis - Symptoms and causes". Mayo Clinic. Retrieved 2018-06-27.
  37. ^ Sharara AI, Aoun E, Abdul-Baki H, Mounzer R, Sidani S, Elhajj I (February 2006). "A randomized double-blind placebo-controlled trial of rifaximin in patients with abdominal bloating and flatulence". The American Journal of Gastroenterology. 101 (2): 326–33. PMID 16454838.
  38. ^ Guslandi M, Petrone MC, Testoni PA (April 2006). "Rifaximin for active ulcerative colitis". Inflammatory Bowel Diseases. 12 (4): 335. doi:10.1097/01.MIB.0000215092.85116.6c. PMID 16633057.
  39. ^ Shafran I, Johnson LK (August 2005). "An open-label evaluation of rifaximin in the treatment of active Crohn's disease". Current Medical Research and Opinion. 21 (8): 1165–9. doi:10.1185/030079905X53252. PMID 16083525.
  40. ^ Weiss GA, Hennet T (August 2017). "Mechanisms and consequences of intestinal dysbiosis" (PDF). Cellular and Molecular Life Sciences. 74 (16): 2959–2977. doi:10.1007/s00018-017-2509-x. PMID 28352996.
  41. ^ Gianotti RJ, Moss AC (November 2016). "The Use and Efficacy of Fecal Microbiota Transplantation for Refractory Clostridium difficile in Patients with Inflammatory Bowel Disease". Inflammatory Bowel Diseases. 22 (11): 2704–2710. doi:10.1097/mib.0000000000000950. PMID 27755271.
  42. ^ Giau VV, Lee H, An SS, Hulme J (June 2019). "Recent advances in the treatment of C. difficile using biotherapeutic agents". Infection and Drug Resistance. 12: 1597–1615. doi:10.2147/IDR.S207572. PMC 6579870. PMID 31354309.
  43. ^ "What is FMT? – The Fecal Transplant Foundation". thefecaltransplantfoundation.org. Retrieved 2018-06-27.
  44. ^ Smith MB, Kelly C, Alm EJ (February 2014). "Policy: How to regulate faecal transplants". Nature. 506 (7488): 290–1. doi:10.1038/506290a. PMID 24558658.
  45. ^ "Fecal Microbiota Transplantation".
  46. ^ Dupont HL (October 2013). "Diagnosis and management of Clostridium difficile infection". Clinical Gastroenterology and Hepatology. 11 (10): 1216–23, quiz e73. doi:10.1016/j.cgh.2013.03.016. PMID 23542332.
  47. ^ Food and Agriculture Organization of the United Nations; World Health Organization. Health and Nutritional Properties of Probiotics in Food Including Powder Milk with Live Lactic Acid Bacteria.Córdoba, Argentina: Food and Agriculture Organization of the United Nations, World Health Organization; 2001.
  48. ^ Drakes M, Blanchard T, Czinn S (June 2004). "Bacterial probiotic modulation of dendritic cells". Infection and Immunity. 72 (6): 3299–309. doi:10.1128/IAI.72.6.3299-3309.2004. PMC 415669. PMID 15155633.
  49. ^ Kim SO, Sheikh HI, Ha SD, Martins A, Reid G (December 2006). "G-CSF-mediated inhibition of JNK is a key mechanism for Lactobacillus rhamnosus-induced suppression of TNF production in macrophages". Cellular Microbiology. 8 (12): 1958–71. doi:10.1111/j.1462-5822.2006.00763.x. PMID 16889627.
  50. ^ Kendall MM, Sperandio V (January 2007). "Quorum sensing by enteric pathogens". Current Opinion in Gastroenterology. 23 (1): 10–5. doi:10.1097/MOG.0b013e3280118289. PMID 17133078.
  51. ^ a b Wischmeyer PE, McDonald D, Knight R (August 2016). "Role of the microbiome, probiotics, and 'dysbiosis therapy' in critical illness". Current Opinion in Critical Care. 22 (4): 347–53. doi:10.1097/MCC.0000000000000321. PMC 5065053. PMID 27327243.
  52. ^ a b Kim SK, Guevarra RB, Kim YT, Kwon J, Kim H, Cho JH, et al. (September 2019). "Role of Probiotics in Human Gut Microbiome-Associated Diseases". Journal of Microbiology and Biotechnology. 29 (9): 1335–1340. doi:10.4014/jmb.1906.06064. PMID 31434172.

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