Skip to main content

Advertisement

SpringerLink
Log in

Gut Microbiome and Colon Cancer: Role of Bacterial Metabolites and Their Molecular Targets in the Host

  • Basic Science Foundations in Colorectal Cancer (J Roper, Section Editor)
  • Published:
Current Colorectal Cancer Reports

Abstract

Purpose of Review

The relationship between colonic bacteria and the host is symbiotic, but how communication between the two partners occurs is just beginning to be understood at the molecular level. Here, we highlight specific products of bacterial metabolism that are present in the colonic lumen and their molecular targets in the host that facilitate this communication.

Recent Findings

Colonic epithelial cells and mucosal immune cells express several cell surface receptors and nuclear receptors that are activated by specific bacterial metabolites, which impact multiple signaling pathways and expression of many genes. In addition, some bacterial metabolites also possess the ability to cause epigenetic changes in these cells via inhibition of selective enzymes involved in the maintenance of histone acetylation and DNA methylation patterns.

Summary

Colonic bacteria communicate with their host with selective metabolites that interact with host molecular targets. This chemical communication underlies a broad range of the biology and function of colonic epithelial cells and mucosal immune cells, which protect against inflammation and carcinogenesis in the colon under normal physiological conditions.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

  1. Luckey T. Introduction to intestinal microecology. Am J Clin Nutr. 1972;25:1292–4.

    CAS  PubMed  Google Scholar 

  2. •• Sender R, Fuchs S, Milo R. Revised estimates for the number of human and bacterial cells in the body. PLoS Biol. 2016;14:e1002533. This paper questions one of the most commonly cited value for the ratio of bacterial cells to human cells and provides a revised estimate of this ratio as ∼1:1 instead of the previous assumed ∼10:1.

    Article  PubMed  PubMed Central  Google Scholar 

  3. Havenaar R. Intestinal health functions of colonic microbial metabolites: a review. Benefic Microbes. 2011;2:103–14.

    Article  CAS  Google Scholar 

  4. Macfarlane GT, Macfarlane S. Bacteria, colonic fermentation, and gastrointestinal health. J AOAC Int. 2012;95:50–60.

    Article  CAS  PubMed  Google Scholar 

  5. Ramakrishna BS. Role of the gut microbiota in human nutrition and metabolism. J Gastroenterol Hepatol. 2013;28 Suppl 4:9–17.

    Article  CAS  PubMed  Google Scholar 

  6. Zeng H, Chi H. Metabolic control of regulatory T cell development and function. Trends Immunol. 2015;36:3–12.

    Article  CAS  PubMed  Google Scholar 

  7. Vipperla K, O’Keefe SJ. The microbiota and its metabolites in colonic mucosal health and cancer risk. Nutr Clin Pract. 2012;27:624–35.

    Article  PubMed  Google Scholar 

  8. Shanahan F. The colonic microbiota in health and disease. Curr Opin Gastroenterol. 2013;29:49–54.

    Article  CAS  PubMed  Google Scholar 

  9. Kovatcheva-Datchary P, Arora T. Nutrition, the gut microbiome and the metabolic syndrome. Best Pract Res Clin Gastroenterol. 2013;27:59–72.

    Article  CAS  PubMed  Google Scholar 

  10. Fukuda S, Ohno H. Gut microbiome and metabolic diseases. Semin Immunopathol. 2014;36:103–14.

    Article  CAS  PubMed  Google Scholar 

  11. • Schroeder BO, Backhed F. Signals from the gut microbiota to distant organs in physiology and disease. Nat Med. 2016;22:1079–89. This is an outstanding review of the literature summarizing the signals from the gut bacteria that travel to distant organs and influence their function in health and disease.

    Article  CAS  PubMed  Google Scholar 

  12. Bhutia YD, Ganapathy V. Short, but smart: SCFAs train T cells in the gut to fight autoimmunity in the brain. Immunity. 2015;43:629–31.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. •• Haghikia A, Jorg S, Duscha A, et al. Dietary fatty acids directly impact central nervous system autoimmunity via the small intestine. Immunity. 2015;43:817–29. This study demonstrates that dietary fatty acids, by modulating gut microbiota and their metabolism, regulate immune cells in the gut, which then travel to the periphery to impact systemic immunity.

    Article  CAS  PubMed  Google Scholar 

  14. Kuhn KA, Stappenbeck TS. Peripheral education of the immune system by the colonic microbiota. Semin Immunol. 2013;25:364–9.

    Article  CAS  PubMed  Google Scholar 

  15. Selkrig J, Wong P, Zhang X, Pettersson S. Metabolic tinkering by the gut microbiome: implications for brain development and function. Gut Microbes. 2014;5:369–80.

    Article  PubMed  PubMed Central  Google Scholar 

  16. Tang WH, Hazen SL. The contributory role of gut microbiota in cardiovascular disease. J Clin Invest. 2014;124:4204–11.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Vamanu E, Pelinescu D, Sarbu I. Compartive fingerprinting of the human microbiota in diabetes and cardiovascular disease. J Med Food. 2016. doi:10.1089/jmf.2016.0085.

    PubMed  Google Scholar 

  18. Blandino G, Inturri R, Lazzara F, et al. Impact of gut microbiota on diabetes mellitus. Diabetes Metab. 2016. doi:10.1016/j.diabet.2016.04.004.

    PubMed  Google Scholar 

  19. Kraneveld AD, Szklany K, de Theije CG, Garssen J. Gut-to-brain axis in autism spectrum disorders: central role for the microbiome. Int Rev Neurobiol. 2016;131:263–87.

    Article  CAS  PubMed  Google Scholar 

  20. Vinolo MA, Rodrigues HG, Nachbar RT, Curi R. Regulation of inflammation by short-chain fatty acids. Nutrients. 2011;3:858–76.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Felice C, Lewis A, Armuzzi A, Lindsay JO, Silver A. Review article: selective histone deacetylase isoforms as potential therapeutic targets in inflammatory bowel diseases. Aliment Pharmacol Ther. 2015;41:26–38.

    Article  CAS  PubMed  Google Scholar 

  22. Thangaraju M, Gopal E, Martin PM, et al. SLC5A8 triggers tumor cell apoptosis through pyruvate-dependent inhibition of histone deacetylases. Cancer Res. 2006;66:11560–4.

    Article  CAS  PubMed  Google Scholar 

  23. Singh N, Thangaraju M, Prasad PD, et al. Blockade of dendritic cell development by bacterial fermentation products butyrate and propionate through a transporter (Slc5a8)-dependent inhibition of histone deacetylases. J Biol Chem. 2010;285:27601–8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Thangaraju M, Cresci GA, Liu K, et al. GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon. Cancer Res. 2009;69:2826–32.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Tazoe H, Otomo Y, Kaji I, et al. Roles of short-chain fatty acids receptors, GPR41 and GPR43 on colonic functions. J Physiol Pharmacol. 2008;59 Suppl 2:252–62.

    Google Scholar 

  26. Ganapathy V, Thangaraju M, Prasad PD, Martin PM, Singh N. Transporters and receptors for short-chain fatty acids as the molecular link between colonic bacteria and the host. Curr Opin Pharmacol. 2013;13:869–74.

    Article  CAS  PubMed  Google Scholar 

  27. Tan J, McKenzie C, Potamitis M, Thorburn AN, Mackay CR, Macia L. The role of short-chain fatty acids in health and disease. Adv Immunol. 2014;121:91–119.

    Article  CAS  PubMed  Google Scholar 

  28. Ganapathy V, Thangaraju M, Gopal E, et al. Sodium-coupled monocarboxylate transporters in normal tissues and in cancer. AAPS J. 2008;10:193–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  29. Marchiq I, Pouyssegur J. Hypoxia, cancer metabolism and the therapeutic benefit of targeting lactate/H+ symporters. J Mol Med. 2016;94:155–71.

    Article  CAS  PubMed  Google Scholar 

  30. Ganapathy V, Thangaraju M, Prasad PD. Nutrient transporters in cancer: relevance to Warburg hypothesis and beyond. Pharmacol Ther. 2009;121:29–40.

    Article  CAS  PubMed  Google Scholar 

  31. Bhutia YD, Babu E, Ramachandran S, Yang S, Thangaraju M, Ganapathy V. SLC transporters as a novel class of tumour suppressors: identity, function and molecular mechanisms. Biochem J. 2016;473:1113–24.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Li H, Myeroff L, Smiraglia D, et al. SLC5A8, a sodium transporter, is a tumor suppressor gene silenced by methylation in human colon aberrant crypt foci and cancers. Proc Natl Acad Sci U S A. 2003;100:8412–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Miyauchi S, Gopal E, Fei YJ, Ganapathy V. Functional identification of SLC5A8, a tumor suppressor down-regulated in colon cancer, as a Na+-coupled transporter for short-chain fatty acids. J Biol Chem. 2004;279:13293–6.

    Article  CAS  PubMed  Google Scholar 

  34. Frank H, Groger N, Diener M, Becker C, Braun T, Boettger T. Lactaturia and loss of sodium-dependent lactate uptake in the colon of SLC5A8-deficient mice. J Biol Chem. 2008;283:24729–37.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. •• Gurav A, Sivaprakasam S, Bhutia YD, Boettger T, Singh N, Ganapathy V. Slc5a8, a Na+-coupled high-affinity transporter for short-chain fatty acids, is a conditional tumour suppressor in colon that protects against colitis and colon cancer under low-fibre dietary conditions. Biochem J. 2015;469:267–78. This study demonstrated a link between the tumor-suppressive function of the short-chain fatty acid transporter SLC5A8 and the dietary fiber content and provided a reasonable explanation as to why Slc5a8-null mice do not show increased risk for colitis and colon cancer under normal dietary conditions.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Cresci GA, Thangaraju M, Mellinger JD, Liu K, Ganapathy V. Colonic gene expression in conventional and germ-free ice with a focus on the butyrate receptor GPR109A and the butyrate transporter SLC5A8. J Gastrointest Sug. 2010;14:449–61.

    Article  Google Scholar 

  37. •• Singh N, Gurav A, Sivaprakasam S, et al. Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. Immunity. 2014;40:128–39. This study demonstrated unequivocally the anti-inflammatory and tumor-suppressive function of the butyrate receptor GPR109A in vivo using Gpr109a-null mice.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  38. Taggart AK, Kero J, Gan X, et al. (D)-β-hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G. J Biol Chem. 2005;280:26649–52.

    Article  CAS  PubMed  Google Scholar 

  39. •• Tan J, KcKenzie C, Vuillermin PJ, et al. Dietary fiber and bacterial SCFA enhance oral tolerance and protect against food allergy through diverse cellular pathways. Cell Rep. 2016;15:2809–24. Here, the authors showed that a high-fiber content in the diet improved oral tolerance and offered protection against food allergy and that deletion of Gpr43 or Gpr109a in mice exacerbated food allergy.

    Article  CAS  PubMed  Google Scholar 

  40. Ang Z, Ding JL. GPR41 and GPR43 in obesity and inflammation—protective or causative? Front Immunol. 2016;7:28.

    Article  PubMed  PubMed Central  Google Scholar 

  41. Tazoe H, Otomo Y, Karaki S, et al. Expression of short-chain fatty acid receptor GPR41 in the human colon. Biomed Res. 2009;30:149–56.

    Article  CAS  PubMed  Google Scholar 

  42. Karaki S, Mitsui R, Hayashi H, et al. Short-chain fatty acid receptor, Gpr43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine. Cell Tissue Res. 2006;324:353–60.

    Article  CAS  PubMed  Google Scholar 

  43. Karaki S, Tazoe H, Hayashi H, et al. Expression of the short-chain fatty acid receptor, GPR43, in the human colon. J Mol Histol. 2008;39:135–42.

    Article  CAS  PubMed  Google Scholar 

  44. Trompette A, Gollwitzer ES, Yadava K, et al. Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis. Nat Med. 2014;20:159–66.

    Article  CAS  PubMed  Google Scholar 

  45. Kime MH, Kang SG, Park JH, Yanagisawa M, Kim CH. Short-chain fatty acids activate GPR41 and GPR43 on intestinal epithelial cells to promote inflammatory responses in mice. Gastroenterology. 2013;145:396–406.

    Article  Google Scholar 

  46. Maslowski KM, Vieira AT, Ng A, et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature. 2009;461:1282–6.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Smith PM, Howitt MR, Panikov N, et al. The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis. Science. 2013;341:569–73.

    Article  CAS  PubMed  Google Scholar 

  48. Masui R, Sasaki M, Funaki Y, et al. G protein-coupled receptor 43 moderates gut inflammation through cytokine regulation from mononuclear cells. Inflamm Bowel Dis. 2013;19:2848–56.

    Article  PubMed  Google Scholar 

  49. Macia L, Tan J, Vieira AT, et al. Metabolite-sensing receptors GPR43 and GPR109A facilitate dietary fibre-induced gut homeostasis through regulation of the inflammasome. Nat Commun. 2015;6:6734.

    Article  CAS  PubMed  Google Scholar 

  50. Sivaprakasam S, Gurav V, Paschall AV, et al. An essential role of Ffar2 (Gpr43) in dietary fibre-mediated promotion of healthy composition of gut microbiota and suppression of intestinal carcinogenesis. Oncogenesis. 2016;5:e238.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  51. Sina C, Gavrilova O, Forster M, et al. G protein-coupled receptor 43 is essential for neutrophil recruitment during intestinal inflammation. J Immunol. 2009;183:7514–22.

    Article  CAS  PubMed  Google Scholar 

  52. Choi SY, Collins CC, Gout PW, Wang Y. Cancer-generated lactic acid: a regulatory, immunosuppressive metabolite? J Pathol. 2013;230:350–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  53. Liu C, Wu J, Zhu J, et al. Lactate inhibits lipolysis in fat cells through activation of an orphan G-protein-coupled receptor. J Biol Chem. 2009;284:2811–22.

    Article  CAS  PubMed  Google Scholar 

  54. Lee DC, Sohn HA, Park ZY, et al. A lactate-induced response to hypoxia. Cell. 2015;161:595–609.

    Article  CAS  PubMed  Google Scholar 

  55. Jakobsdottir G, Xu J, Molin G, Ahme S, Nyman M. High-fat diet reduces the formation of butyrate, but increases succinate, inflammation, liver fat and cholesterol in rats, while dietary fibre counteracts these effects. PLoS One. 2013;8:e80476.

    Article  PubMed  PubMed Central  Google Scholar 

  56. Yang M, Pollard PJ. Succinate: a new epigenetic hacker. Cancer Cell. 2013;23:709–11.

    Article  CAS  PubMed  Google Scholar 

  57. Boulahbel H, Duran RV, Gottlieb E. Prolyl hydroxylases as regulators of cell metabolism. Biochem Soc Trans. 2009;37:291–4.

    Article  CAS  PubMed  Google Scholar 

  58. He W, Miao FJ, Lin DC, et al. Citric acid cycle intermediates as ligands for orphan G-protein-coupled receptors. Nature. 2004;429:188–93.

    Article  CAS  PubMed  Google Scholar 

  59. Hubbard TD, Murray IA, Perdew GH. Indole and tryptophan metabolism: endogenous and dietary routes to Ah receptor activation. Drug Metab Dispos. 2015;43:1522–35.

    Article  PubMed  PubMed Central  Google Scholar 

  60. Jin UH, Lee SO, Sridharan G, et al. Microbiome-derived tryptophan metabolites and their aryl hydrocarbon receptor-dependent agonist and antagonist activities. Mol Pharmacol. 2014;85:777–88.

    Article  PubMed  PubMed Central  Google Scholar 

  61. Wikoff WR, Anfora AT, Liu J, et al. Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proc Natl Acad Sci U S A. 2009;106:3698–703.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  62. Venkatesh M, Mukherjee S, Wang H, et al. Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. Immunity. 2014;41:296–310.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Stockinger B, Di Meglio P, Gialitakis M, Duarte JH. The aryl hydrocarbon receptor: multitasking in the immune system. Annu Rev Immunol. 2014;32:403–32.

    Article  CAS  PubMed  Google Scholar 

  64. Xie G, Raufman JP. Role of the aryl hydrocarbon receptor in colon neoplasia. Cancers. 2015;7:1436–46.

    Article  PubMed  PubMed Central  Google Scholar 

  65. Goettel JA, Gandhi R, Kenison JE, et al. AHR activation is protective against colitis driven by T cells in humanized mice. Cell Rep. 2016;17:1318–29.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  66. Diaz-Diaz CJ, Ronnekleiv-Kelly SM, Nukaya M, Geiger PG, et al. The aryl hydrocarbon receptor is a repressor of inflammation-associated colorectal tumorigenesis in mouse. Ann Surg. 2016;264:429–36.

    Article  PubMed  Google Scholar 

  67. Pondugula SR, Pavek P, Mani S. Pregnane X receptor and cancer: context-specificity is key. Nucl Receptor Res. 2016;3.

  68. Jonker JW, Liddle C, Downes M. FXR and PXR: potential therapeutic targets in cholestasis. J Steroid Biochem Mol Biol. 2012;130:147–58.

    Article  CAS  PubMed  Google Scholar 

  69. •• Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med. 2013;19:576–85. This was the first report on the generation of trimethylamine (TMA) in the colon by bacterial metabolism of diet-derived carnitine and the subsequent hepatic conversion of TMA into the cardiovascular toxin TMA oxide, thus providing a mechanistic link between high dietary intake of carnitine-rich red meat and risk for cardiovascular disease.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  70. • Tang WH, Wang Z, Levison BS, et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. N Engl J Med. 2013;368:1575–84. This study provides evidence for the association between increased plasma levels of TMAO and risk for cardiovascular disease and also for dietary lipid phosphatidylcholine as the source for colonic bacterial metabolism to generate TMA, the precursor for TMAO.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  71. Gregory JC, Buffa JA, Org E, et al. Transmission of atherosclerosis susceptibility with gut microbial transplantation. J Biol Chem. 2015;290:5647–60.

    Article  CAS  PubMed  Google Scholar 

  72. Brown JM, Hazen SL. The gut microbial endocrine organ: bacterially derived signals driving cardiometabolic diseases. Annu Rev Med. 2015;66:343–59.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  73. Wilson A, McLean C, Kim RB. Trimethylamine-N-oxide: a link between the gut microbiome, bile acid metabolism, and atherosclerosis. Curr Opin Lipidol. 2016;27:148–54.

    Article  CAS  PubMed  Google Scholar 

  74. Wallrabenstein I, Kuklan J, Weber L, et al. Human trace amine-associated receptor TAAR5 can be activated by trimethylamine. PLoS One. 2013;8. e54950.

  75. Lakhan R, Said M. Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for casein kinase 2-mediated pathway. Am J Physiol Cell Physiol. 2017. doi:10.1152/ajpcell.00300.2016.

    PubMed  Google Scholar 

  76. Anitha M, Vijay-Kumar M, Sitaraman SV, Gewirtz AT, Srinivasan S. Gut microbial products regulate murine gastrointestinal motility via Toll-like receptor 4 signaling. Gastroenterology. 2012;143:1006–16.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  77. Reichardt F, Chassaing B, Nezami BG, et al. Western diet induces colonic nitrergic myenteric neuropathy and dysmotility in mice via saturated fatty acid- and LPS-induced TLR4 signaling. J Physiol. 2016. doi:10.1113/JP273269.

    Google Scholar 

  78. Cario E. Microbiota and innate immunity in intestinal inflammation and neoplasia. Curr Opin Gastroenterol. 2013;29:85–91.

    Article  CAS  PubMed  Google Scholar 

  79. Kamba A, Lee IA, Mizoguchi E. Potential association between TLR4 and chitinase 3-like 1 (CHI3L1/YKL40) signaling on colonic epithelial cells in inflammatory bowel disease and colitis-associated cancer. Curr Mol Med. 2013;13:1110–21.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  80. Jiang Q, Akashi S, Miake K, Petty HR. Lipopolysaccharide induces physical proximity between CD14 and Toll-like receptor 4 (TLR4) prior to nuclear translocation of NF-κB. J Immunol. 2000;165:3541–4.

    Article  CAS  PubMed  Google Scholar 

  81. de Silva Correia J, Soldau K, Christen U, Tobias PS, Ulevitch RJ. Lipopolysaccharide is close proximity to each of the proteins in its membrane receptor complex; transfer from CD14 to TLR4 and MD2. J Biol Chem. 2001;276:21129–35.

    Article  Google Scholar 

  82. •• Kuo WT, Lee TC, Yang HY, et al. LPS receptor subunits have antagonistic roles in epithelial apoptosis and colonic carcinogenesis. Cell Death Diff. 2015;22:1590–604. This study provided the molecular rationale for the antagonistic actions of LPS in colonic epithelium via the presence or absence of the co-expression of CD14 with TLR4.

    Article  CAS  Google Scholar 

  83. Ishida A, Akita K, Mori Y, et al. Negative regulation of Toll-like receptor-4 signaling through the binding of glycosylphosphatidylinositol-anchored glycoprotein, CD14, with the sialic acid-binding lectin, CD33. J Biol Chem. 2014;289:25341–50.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  84. Santaolalla R, Sussman DA, Ruiz JR, et al. TLR4 activates the β-catenin pathway to cause intestinal neoplasia. PLoS One. 2013;8:e63298.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  85. Munford RS, Hall CL. Detoxification of bacterial lipopolysaccharide (endotoxins) by a human neutrophil enzyme. Science. 1986;234:203–5.

    Article  CAS  PubMed  Google Scholar 

  86. • Janelsins BM, Lu M, Datta SK. Altered inactivation of commensal LPS due to acyloxyacyl hydrolase deficiency in colonic dendritic cells impairs mucosal Th17 immunity. Proc Natl Acad Sci U S A. 2014;111:373–8. This study describes the role of chronic exposure of the colon to LPS in the polarization of naïve T cells towards pro-inflammatory Th17-positive T cells or immunosuppressive regulatory T cells (Tregs).

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX, 79430, USA

    Yangzom D. Bhutia, Jiro Ogura, Sathish Sivaprakasam & Vadivel Ganapathy

Authors
  1. Yangzom D. Bhutia
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Jiro Ogura
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Sathish Sivaprakasam
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Vadivel Ganapathy
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Vadivel Ganapathy.

Ethics declarations

Conflict of Interest

The authors declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

All reported studies/experiments with human or animal subjects performed by the authors have been previously published and complied with all applicable ethical standards, including the Helsinki declaration and its amendments, institutional/national research committee standards, and international/national/institutional guidelines. The data reported as “unpublished” were from animal studies performed with approval from the Institutional Animal Care and Use Committee.

Funding Support

This work was supported by the National Institutes of Health, Grant No. CA190710, and by the Welch Endowed Chair in Biochemistry, Grant No. BI-0028, at the Texas Tech University Health Sciences Center.

Additional information

This article is part of the Topical Collection on Basic Science Foundations in Colorectal Cancer

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Bhutia, Y.D., Ogura, J., Sivaprakasam, S. et al. Gut Microbiome and Colon Cancer: Role of Bacterial Metabolites and Their Molecular Targets in the Host. Curr Colorectal Cancer Rep 13, 111–118 (2017). https://doi.org/10.1007/s11888-017-0362-9

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11888-017-0362-9

Keywords

Search

Navigation