Role of Oral Microorganism in Oral and Gastrointestinal Cancer Risk

The NIH Human Microbiome Venture, propelled as a piece of the NIH Guide for Restorative Exploration, indicated the need to quicken our comprehension of how our bodies and microorganisms communicate to impact wellbeing and malady (Peterson, et. al., 2009). It is conjectured that the human microbiome is related with human wellbeing and that dysbiosis can prompt an assortment of illnesses. Up to this point, investigations of the human microflora have been founded on bacterial culture, which we presently know is constrained and inhumane, in light of the fact that substantial quantities of nonculturables (up to 80%) can't be considered in culture (Chen, et. al., 2010), (Dewhirst, et. al., 2010). The improvement of high-throughput hereditary based microbiome measures sped up concentrates to completely look at the human microbiome, the totality of human micro flora, including nonculturable creatures. With regards to these improvements, it is getting to be conceivable to test the speculation that the oral microbiome and its irregular characteristics are related etiologically with cancers of the oral and gastrointestinal tracts.

It is entrenched that oral microscopic organisms are basic to the improvement of periodontal ailment and tooth misfortune (Pihlstrom, et. al., 2005), and these oral sicknesses have been connected in various investigations to the danger of oral and gastrointestinal cancer, with the most steady expanded dangers noted in investigations of oral and esophageal cancer, trailed by prove for pancreatic and gastric cancer (checked on in (Meyer, et. al., 2008) (Fitzpatrick & Katz, 2010); these connections tend to continue in the wake of considering frustrating variables—e.g., smoking, weight list, and financial status (Meyer, et. al., 2008), (Fitzpatrick & Katz, 2010) (Michaud, et. al., 2008) (Hujoel, et. al., 2003) (Hiraki, et. al., 2008). The hidden component for the relationship between oral wellbeing status and these cancer isn't totally seen, yet it is conceivable that these relationship of cancer with oral ailment may mirror a more grounded fundamental relationship of disease with so far unexamined oral microbiome profiles.

Oral microflora may influence oral and gastrointestinal cancer hazard by neighborhood enactment of liquor and smoking-related cancer-causing agents, two settled hazard factors for oral and certain gastrointestinal disease composes (Schottenfeld & Fraumeni, 2006). While ethanol (liquor) itself isn't unequivocally cancer-causing, oral microscopic organisms have the ability to change over ethanol to acetaldehyde, which is an in vitro (Wang, et. al., 2000) and in vivo genotoxin (Langevin, et. al., 2011) and perceived human

following liquor utilize (Fig. 1) (Salaspuro, 2009). Mutagenic measures of acetaldehyde can be identified in salivation after ingestion of direct dosages of ethanol, while flushing the mouth with antibacterial chlorhexidine before ethanol presentation lessens salivary acetaldehyde levels by half, in parallel with a checked diminishing in microorganism tallies (Homann, et. al., 1997). Likewise, oral microscopic organisms may assume a part in expanded enactment of cancer-causing nitrosamines from tobacco smoking (Yang, et. al., 2011); in vitro normal oral microorganisms actuate the tobacco smoke nitrosamine, nitrosodiethylamine (NDEA), to its cancer-causing (IARC, Gathering 2A), adduct-framing hydroxylated item (Verna, et. al., 1996). A part for oral microorganisms in cancer-causing agent digestion is additionally bolstered by perception that oral germicide mouthwash treatment (chlorhexidine) fundamentally diminishes nitrosoamino corrosive arrangement and discharge in salivation (locally) and pee (foundationally; each by around 30%) (Shapiro, et. al., 1991). Smoking likewise potentiates the liquor related creation of acetaldehyde by oral microscopic organisms (Salaspuro, 2009), conceivably adding to liquor tobacco cooperation‘s in carcinogenesis. Taken together, this information recommends oral microbial potential for neighborhood digestion of liquor and smoking-related cancer-causing agents and a potential part in oral and gastrointestinal carcinogenesis.

Relationship of periodontal illness and tooth misfortune with cancer at removed locales, including stomach (Abnet, et. al., 2005), (Abnet, et. al., 2001) and pancreas cancer (Hujoel, et. al., 2003), (Michaud, et. al., 2007), (Stolzenberg-Solomon, et. al., 2003), recommend that foundational systems may likewise be engaged with oral microbiome-related carcinogenesis. It is winding up progressively certain that periodontal infection is related with foundational impacts (Lamster, et. al., 2008), (Pizzo, et. al., 2010), incorporating predictable associations with cardiovascular illness (Kebschull, et. al., 2010) and diabetes (Pizzo, et. al., 2010). Oral microbes were found in atherosclerotic plaque, and imperatively, fruitful treatment for periodontal illness, prompts inversion of fundamental markers for these sicknesses, including enhanced endothelial capacity (Tonetti, et. al., 2007), diminish in incendiary markers (Tonetti, et. al., 2007), (Li, et. al., 2011), (Moura, et. al., 2010), and enhanced glycemic control in diabetics (Teeuw, et. al., 2010), giving solid confirmation that periodontal ailment is causally connected with these foundational impacts. Albeit oral and gut microbiome network structures contrast in similar people (Koren, et. al., 2011), certain oral microscopic organisms can achieve the GI tract (Ahn unpublished information). Then again, oral microbes are wellsprings of rehashed transient fundamental 2008) (Olsen, 2008). Moreover, microscopic organisms can give a wellspring of ligands to toll-like receptors (TLRs) (Chinen, et. al., 2010) at target organ film receptors; TLRs are receptors on natural safe cells that predicament fundamentally saved particles got from microorganisms, all in all indicated pathogen-related atomic examples (PAMPs), and along these lines possibly connect fiery reaction and downstream cell motioning to a wide range of human microbes. Proof is building that irritation because of immunologic reaction to constant introduction to microorganisms and their poisons may assume a critical part in oral and gastrointestinal carcinogenesis (Pizzo, et. al., 2010), (Meurman, 2010), (Rogers Abdominal Muscle & Fox, 20064)

The oral hole gives an assorted variety of situations to bacterial networks and thusly microbiome profiles vary for different intraoral surfaces. The microflora of subgingival and supragingival plaque disciple to tooth structure have a tendency to be comparative, in spite of the fact that anaerobes have a tendency to prevail subgingivally. There is likewise fluctuation in microflora of the dorsal and parallel tongue and between epithelial covering of delicate and hard tissues (Mager, et. al., 2003). Salivary microbial profiles have a tendency to mirror the pervasiveness of bacterial pathogens in disciple oral biofilms and to be related with chance for dental ailment and pathogen transmission between people; likewise, a lessening in the salivary tally of pathogens can fill in as a pointer of remedial adequacy in the treatment of oral ailment (Spaces & Openings, 2000). Consequently, salivary microbial evaluation may fill in as a surrogate example hotspot for oral pathogens identified with cancer hazard.

Huge advances have been made in research facility examine for hereditary based microbiome appraisal, free of bacterial culture (Pozhitkov, et. al., 2000). Current high-throughput approaches utilize hereditary groupings of 16S ribosomal RNA (or 16S rRNA), a part of the 30S subunit of prokaryotic ribosome. 16S rRNA is utilized as a part of hereditary microbiome measure since segments of this succession are exceedingly rationed between various types of microscopic organisms and archaea, while other write particular segments are very factor. 16S rRNA structure is utilized in the terminal confinement section length polymorphism

hybridization, and in 16S rRNA sequencing. Terminal confinement part length polymorphism (TRFLP) is a sub-atomic profiling of microbial networks in light of the situation of a limitation site nearest to a named end of the opened up 16S rRNA quality (Sanders, 2010). Following PCR of the16S rRNA quality, the blend of amplicons is subjected to a confinement response. The blend of sections is isolated utilizing either slim or polyacrylamide electrophoresis and the sizes of the diverse terminal parts are controlled by fluorescence recognition. This technique is a rough method to analyze the sub-atomic profiles of bacterial networks; in any case, it isn't reasonable for the distinguishing proof of particular microscopic organisms. A further constraint is that any two particular groupings which share a terminal limitation site will bring about one pinnacle and will be indistinct. 16S rRNA quality pyrosequencing and the Human Oral Microorganism Distinguishing proof Microarray (HOMIM) (Colombo, et. al., 2009) are two regular high-throughput oral microbiome examines that give rich microbiome appraisal past the limit of RFLPs. HOMIM utilizes uniquely planned tests to recognize ~ 300 of the most pervasive oral bacterial species. Since this technique depends on a preconstructed microarray, the network structure recognized is restricted to the particular hybridization tests chose for already distinguished bacterial DNA arrangements, yet it has the benefits of lower cost and institutionalized information examination. 16S rRNA quality pyrosequencing is an expansive based sequencing approach, utilizing PCR preliminaries to exceedingly rationed districts for intensification of a section of the 16S rRNA quality, trailed by DNA pyrosequencing to recognize exceptional grouping peruses. Contrasted with customary sequencing strategies like Sanger sequencing, pyrosequencing gives a bigger number of peruses and more prominent profundity of scope in a cost-productive way. Despite the fact that pyrosequencing from 454 or Illumina give shorter peruses than Sanger sequencing, this cutting edge sequencing technique is a noteworthy progress to create high-throughput, hugely parallel handled sequencing, permitting the discovery of more noteworthy microbial assorted variety because of the extensive number of peruses and more prominent scope profundity. We found that human oral microbiome network profiles surveyed by 16S rRNApyrosequencing and HOMIM were exceedingly associated at the phylum level and, for the more typical taxa, at the family level (Ahn, et. al., 2011). In spite of the fact that the pyrosequencing strategy recognizes a more prominent number of uncommon genera, this differential may not be conclusive in direct estimated epidemiologic dangers related with generally uncommon exposures. We consider the two strategies as of now appropriate for high-throughput epidemiologic examinations relating the oral microbiome to illness chance (Ahn, et. al., 2011). Notwithstanding strategies utilizing 16S rRNA quality assorted variety for ordered characterization by bacterial sort, it is getting to be taken a toll productive to arrangement the whole genomic material in tests, permitting the get together of entire microbiome networks, including the capacity to evaluate practical and phenotypic connections for quality families (Petrosino, et. al., 2009). On account of sequencing costs, computational difficulties, and the distinguishing proof of new genomic arrangements with either obscure capacity or low quality comment (Preza, et. al., 2009), these investigations are right now constrained fundamentally to little scale investigations. This metagenomic approach is still being developed for expansive scale contemplates. The upsides and downsides of 16S rRNApyrosequencing, HOMIM, and metagenomic sequencing are abridged in Table 1.

arrangement to the reference rRNA database and further characterization by scientific categorization. The Human Oral Microbiome Database (HOMD http://www.homd.org/) and 16S rRNA quality reference arrangements, for example, RDP (http://rdp.cme.msu.edu/) and Silva (http://www.arb-silva.de/) are as of now accessible (Chen, et. al., 2010). We have as of late described 11 bacterial phyla and 77 genera in human salivary examples utilizing the 16S rRNA quality pyrosequencing examine, in light of RDP (Ahn, et. al., 2011). Of these phyla, five (Firmicutes, Proteobacteria, Bacteroidetes, Actinobacteria, and Fusobacteria) prevailed (99%). Relative plenitude of phyla and the 25 most regular genera are appeared in Fig. 2.

Oral microbiome profiles tend to indicate examples of relative intraindividual solidness after some time and clear interindividual contrasts. One investigation inspected fleeting security utilizing 4 rehashed oral microbiome profiles estimated up to a half year separated from similar people and discovered examples from same subject bunched, proposing stable microbial profiles after some time (Costello, et. al., 2009). These discoveries were likewise reproduced in another examination (Lazarevic, et. al., 2010). We likewise watched interindividual differentials in the oral microbiome in 20 subjects. The desire for high worldly soundness and considerable interindividual fluctuation in the creation of individual bacterial networks is right now likewise being assessed for measurable distinguishing proof (Fierer, et. al., 2010). Huge interindividual oral microbiome differentials have likewise been appeared for bunches portrayed by periodontal ailment (Colombo, et. al., 2009) and root caries (Preza, et. al., 2009). The relative intraindividual steadiness after some time and phenotypes.

High-throughput microbiome examine innovation has opened the entryway for "microbiomic" the study of disease transmission; beginning endeavors have given testable speculations utilizing these high-throughput microbiome measures, relating the oral microbiome to chance for oral cancer (Yang, et. al., 2011) and esophageal microbiome to premalignant Barrett's throat (Yang, et. al., 2009). analyzed whether throat microbiome is related with esophagitis and Barrett's throat in tissue tests from 34 subjects. They recognized a "sort I" microbiome overwhelmed by the family Streptococcus and amassed in the typical throat and a "sort II" microbiome containing a more noteworthy extent of gram-negative anaerobes/microaerophiles and essentially corresponded with esophagitis (OR = 15.4) and Barrett's throat (OR = 16.5), proposing the attainability to arrange microbiome related with this premalignant illness. In a little case-control investigation of oral microbiome with oral cancer (Yang, et. al., 2011) (10 cases and 10 controls), oral squamous cell cancer/leukoplakia was related with an obvious decline in the relative wealth of streptococcus (22.3%) contrasted and nonsmoking (39.4%) and smoking controls (40.1%). While beginning advances are promising [51], multi-disciplinary joint efforts in the study of disease transmission, microbiology, hereditary qualities, immunology, and bioinformatics will be expected to widen our comprehension of the relationship of oral microscopic organisms to cancer hazard (Peterson, et. al., 2009). Building up the relationship of the oral microbiome with cancer may prompt noteworthy advances in comprehension of cancer etiology, conceivably opening another exploration worldview for these infections. The distinguished oral bacterial profiles may likewise fill in as promptly available, noninvasive biomarkers for the ID of high hazard for cancer, supplementing known hazard factors for these illnesses. In the event that these connections are affirmed as causal, discoveries may likewise prompt microbial prophylactic cancer anticipation in clinical practice.

REFERENCES

Abnet C.C., Kamangar F., Dawsey S.M., Stolzenberg-Solomon R.Z., Albanes D., et. al. (2005). Tooth misfortune is related with expanded danger of gastric non-cardia adenocarcinoma in a partner of Finnish smokers. Scand J Gastroenterol; 40: pp. 681-687. [PubMed: 16036528]

P.R., et. al. (2001). Imminent investigation of tooth misfortune and occurrence esophageal and gastric cancer in China. Cancer Causes Control.2001; 12: pp. 847-854. [PubMed: 11714113] Ahn J., Yang Y., Paster B.J., Ganly I., Morris L., et. al. (2011). Oral microbiome profiles: 16S rRNApyrosequencing and microarray measure examination. PLoS One. 2011; 6: pp. e22788-e22795. [PubMed: 21829515] Bahrani-Mougeot F.K., Paster B.J., Coleman S., Ashar J., Barbuto S., et. al. (2008) Different and novel oral bacterial species in blood following dental systems. J Clin Microbiol.2008; 46: pp. 2129-2132. [PubMed: 18434561] Chen T., Yu W.H., Izard J., Baranova O.V., Lakshmanan A.N., et. al. (2010). The human oral microbiome database: a web available asset for researching oral microorganism ordered and genomic data. Database (Oxford): baq013. Chinen T., Volchkov P.Y., Chervonsky A.V., Rudensky A.Y. (2010). A basic part for administrative Immune system microorganism intervened control of aggravation without commensal microflora. J Exp Med. 2010; 207: pp. 2323-2330. [PubMed: 20921284] Colombo A.P., Boches S.K., Cotton S.L., Goodson J.M., Kent R., et. al. (2009). Examinations of subgingival microbial profiles of obstinate periodontitis, extreme periodontitis, and periodontal wellbeing utilizing the human oral organism distinguishing proof microarray. J Periodontol; 80: pp. 1421-1432. [PubMed: 19722792] Costello E.K., Lauber C.L., Hamady M., Fierer N., Gordon J.I., et. al. (2009). Bacterial people group variety in human body natural surroundings crosswise over space and time. Science.2009; 326: pp. 1694-1697. [PubMed: 19892944] Crasta K., Daly C.G., Mitchell D., Curtis B., Stewart D., et. al. (2006). Bacteraemia because of dental flossing. J ClinPeriodontol.2009; 36: pp. 323-332. [PubMed: 19426179] Dewhirst F.E., Chen T., Izard J., Paster B.J. (2010). Leather expert air conditioning, et al. The human oral microbiome.J Bacteriol.2010; 192: pp. 5002-5017. [PubMed: 20656903] E.K., et. al. (2010). Scientific recognizable proof utilizing skin bacterial networks. ProcNatlAcadSci USA. 2010; 107: pp. 6477-6481. [PubMed: 20231444] Fitzpatrick S.G., Katz J. (2010). The relationship between periodontal infection and disease: a survey of the writing. J. Gouge. 2010; 38: pp. 83-95. [PubMed: 19895866] Hiraki A., Matsuo K., Suzuki T., Kawase T., Tajima K. (2008). Teeth misfortune and danger of cancer at 14 basic destinations in Japanese. Cancer Epidemiol Biomarkers Prev. 2008; 17: pp. 1222-1227. [PubMed: 18483345] Homann N., Jousimies-Somer H., Jokelainen K., Heine R., Salaspuro M. (1997). High acetaldehyde levels in salivation after ethanol utilization: methodological viewpoints and pathogenetic suggestions. Carcinogenesis; 18: pp. 1739-1743. [PubMed: 9328169] Hujoel P.P., Drangsholt M., Spiekerman C., Weiss N.S. (2003). An investigation of the periodontitis-cancer affiliation. Ann Epidemiol. 2003; 13: pp. 312-316. [PubMed: 12821269] IARC (1999). Monographs on the assessment of cancer-causing dangers to people; re-assessment of some natural synthetic compounds, hydrazine and hydrogen peroxide. Iwai T. (2009). Periodontal bacteremia and different vascular maladies. J Periodontal Res. 2009; 44: pp. 689-694. [PubMed: 19874452] Kebschull M., Demmer R.T., Papapanou P.N. (2010). "Gum bug, allow my heart to sit unbothered!"— epidemiologic and unthinking proof connecting periodontal diseases and atherosclerosis. J Gouge Res. 2010; 89: pp. 879-902. [PubMed: 20639510] Koren O., Spor A., Felin J., Fak F., Stombaugh J., et. al. (2011). Microorganisms and wellbeing sackler colloquium: human oral, gut, and plaque microflora in patients with atherosclerosis. ProcNatlAcadSci USA. 2011; 108: pp. 4592-4598. [PubMed: 20937873] Lamster I.B., DePaola D.P., Oppermann R.V., Papapanou P.N., More stunning R.S. (2008). The relationship of periodontal sickness to ailments and disarranges at inaccessible locales: correspondence to social insurance

Langevin F., Crossan G.P., Rosado I.V., Arends M.J., Patel K.J. (2011). Fancd2 checks the lethal impacts of normally created aldehydes in mice. Nature.2011; 475: pp. 53-58. [PubMed: 21734703] Lazarevic V., Whiteson K., Hernandez D., Francois P., Schrenzel J. (2010). Investigation of between and intra-individual varieties in the salivary microflora. BMC Genomics.2010; 11: pp. 523. [PubMed: 20920195] Li X., Tse H.F., Yiu K.H., Li L.S., Jin L. (2011). Impact of periodontal treatment on coursing CD34(+) cells and fringe vascular endothelial capacity: a randomized controlled preliminary. J ClinPeriodontol.2011; 38: pp. 146-156. Lockhart P.B., Brennan M.T., Sasser H.C., Fox P.C., Paster B.J., et. al. (2008). Bacteremia related with toothbrushing and dental extraction. Dissemination.2008; 117: pp. 3118-3125. [PubMed: 18541739] Mager D.L., Ximenez-Fyvie L.A., Haffajee Promotion, Socransky S.S. (2003). Appropriation of chose bacterial species on intraoral surfaces. J ClinPeriodontol; 30: pp. 644-654. [PubMed: 12834503] Meurman J. (2010). Oral microflora and cancer. J Oral Microbiol; 2: pp. 1-10. Meyer M.S., Joshipura K., Giovannucci E., Michaud D.S. (2008). An audit of the connection between tooth misfortune, periodontal illness, and Cancer. Cancer Causes Control.2008; 19: pp. 895-907. [PubMed: 18478344] Michaud D.S., Joshipura K., Giovannucci E., Fuchs C.S. (2007). An imminent investigation of periodontal sickness and pancreatic cancer in US male wellbeing experts.J Natl Disease Inst. 2007; 99: pp. 171-175. [PubMed: 17228001] Michaud D.S., Liu Y., Meyer M., Giovannucci E., Joshipura K. (2008). Periodontal malady, tooth misfortune, and cancer hazard in male wellbeing experts: a forthcoming accomplice think about. Lancet Oncol.2008; 9: pp. 550-558. [PubMed: 18462995] Moura Foz A.N., Alexandre Romito G., Manoel Bispo C., Luciancencov Petrillo C., Patel K. et. al. (2010). Periodontal treatment and biomarkers identified with cardiovascular hazard. Minerva Stomatol; 59: pp. 271-283. [PubMed: 20502435] Peterson J., Garges S., Giovanni M., McInnes P., Wang L., et. al. (2009). The NIH human microbiome venture.Genome Res. 2009; 19: pp. 2317-2323. [PubMed: 19819907] Petrosino J.F., Highlander S., Luna R.A., Gibbs R.A., Versalovic J. (2009). Metagenomicpyrosequencing and microbial recognizable proof. Clin Chem. 2009; 55: pp. 856-866. [PubMed: 19264858] Pihlstrom B.L., Michalowicz B.S., Johnson N.W. (2005). Periodontal ailments. Lancet.2005; 366: pp. 1809-1820. [PubMed: 16298220] Pizzo G., Guiglia R., Lo Russo L., Campisi G. (2010). Dentistry and inward drug: from the central disease hypothesis to the periodontal medication idea. Eur J Assistant Med. 2010; 21: pp. 496-502. [PubMed: 21111933] Pozhitkov A.E., Beikler T., Flemmig T. (2000). Honorable Dad. High-throughput strategies for investigation of the human oral microbiome.Periodontol.2011; 55: pp. 70-86. Preza D., Olsen I., Willumsen T., Boches S.K., Cotton S.L., et. al. (2009). Microarray investigation of the microflora of root caries in elderly. Eur J ClinMicrobiol Contaminate Dis. 2009; 28: pp. 509-517. [PubMed: 19039610] Rogers Abdominal Muscle, Fox J.G. (20064). Aggravation and Cancer I. Rat models of irresistible gastrointestinal and liver disease. Am J PhysiolGastrointest Liver Physiol; 286: pp. G361-G366. [PubMed: 14766534] Salaspuro M. (2009). Acetaldehyde: a combined cancer-causing agent in people. Compulsion.2009; 104: pp. 551-553. [PubMed: 19335653] Sanders, E.R. (2010). Mill Operator, J,H., Herbold, C. I. Microbiologist, a disclosure based course in microbial biology and sub-atomic advancement. Washington: ASM press. Schottenfeld D., Fraumeni, J.F. (2006). Cancer the study of disease transmission and counteractive action.Vol. section 13. New York: Oxford College Press; 2006. liquor and section 14, Tobacco.

Quantitative connection between oral nitrate-diminishing action and the endogenous arrangement of N-nitrosoamino acids in people.Nourishment ChemToxicol.1991; 29: pp. 751-755. [PubMed: 1761254] Spaces J., Openings H. (2000). Bacterial and viral pathogens in salivation: sickness relationship and irresistible hazard. Periodontol.2011; 55: pp. 48-69. Stolzenberg-Solomon R.Z., Dodd K.W., Blaser M.J., Virtamo J., Taylor P.R., et. al. (2003). Tooth misfortune, pancreatic cancer, and Helicobacter Pylori. Am J ClinNutr.2003; 78: pp. 176-181. [PubMed: 12816788] Teeuw W.J., Gerdes V.E., Loos B.G. (2010). Impact of periodontal treatment on glycemic control of diabetic patients: a deliberate survey and meta-examination. Diabetes Care.2010; 33: pp. 421-427. [PubMed: 20103557] Tonetti M.S., D'Aiuto F., Nibali L., Donald A., Storry C., et. al. (2007). Treatment of periodontitis and endothelial capacity. N Engl J Med. 2007; 356: pp. 911-920. [PubMed: 17329698] Verna L., Whysner J., Williams G.M. (1996). N-nitrosodiethylamine robotic information and hazard evaluation: bioactivation, DNA-adduct arrangement, mutagenicity, and cancer commencement. PharmacolTher. 1996; 71: pp. 57-81. [PubMed: 8910949] Wang M., McIntee E.J., Cheng G., Shi Y., Villalta P.W., et. al. (2000). Recognizable proof of DNA adducts of acetaldehyde. Chem Res Toxicol.2000; 13: pp. 1149-1157. [PubMed: 11087437] Yang L., Ganly I., Morris L., Palmer F., Deng H., et. al. (2011). Importance of microbiome to cigarette smoking and oral cancer. J Scratch Res. 2011; 90: pp. 120. Yang L., Lu X., Nossa C.W., Francois F., Look R.M., et. al. (2009). Irritation and intestinal metaplasia of the distal throat are related with modifications in the microbiome. Gastroenterology; 137: pp. 588-597. [PubMed: 19394334]

M.Sc. Microbiology