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Colon
Original article
Race-dependent association of sulfidogenic bacteria with colorectal cancer
  1. Cemal Yazici1,
  2. Patricia G Wolf2,
  3. Hajwa Kim3,
  4. Tzu-Wen L Cross2,
  5. Karin Vermillion2,
  6. Timothy Carroll1,
  7. Gaius J Augustus4,
  8. Ece Mutlu5,
  9. Lisa Tussing-Humphreys6,
  10. Carol Braunschweig7,
  11. Rosa M Xicola8,
  12. Barbara Jung1,
  13. Xavier Llor8,
  14. Nathan A Ellis4,
  15. H Rex Gaskins2,9
  1. 1Division of Gastroenterology and Hepatology, University of Illinois College of Medicine at Chicago, Chicago, Illinois, USA
  2. 2Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
  3. 3Center for Clinical and Translational Science, University of Illinois at Chicago, Chicago, Illinois, USA
  4. 4Department of Cellular and Molecular Medicine, University of Arizona, Tucson, Arizona, USA
  5. 5Division of Digestive Diseases and Nutrition, Rush University Medical Center, Chicago, Illinois, USA
  6. 6Division of Academic Internal Medicine and Geriatrics, University of Illinois College of Medicine at Chicago, Chicago, Illinois, USA
  7. 7Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA
  8. 8Section of Digestive Diseases, Yale University, New Haven, Connecticut, USA
  9. 9Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
  1. Correspondence to Dr H. Rex Gaskins, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801, USA; hgaskins{at}illinois.edu OR Dr Nathan A Ellis, University of Arizona Cancer Center, 1515 N Campbell Ave, Tucson, AZ 85724, USA; naellis{at}email.arizona.edu

Abstract

Objective Colorectal cancer (CRC) incidence is higher in African Americans (AAs) compared with non-Hispanic whites (NHWs). A diet high in animal protein and fat is an environmental risk factor for CRC development. The intestinal microbiota is postulated to modulate the effects of diet in promoting or preventing CRC. Hydrogen sulfide, produced by autochthonous sulfidogenic bacteria, triggers proinflammatory pathways and hyperproliferation, and is genotoxic. We hypothesised that sulfidogenic bacterial abundance in colonic mucosa may be an environmental CRC risk factor that distinguishes AA and NHW.

Design Colonic biopsies from uninvolved or healthy mucosa from CRC cases and tumour-free controls were collected prospectively from five medical centres in Chicago for association studies. Sulfidogenic bacterial abundance in uninvolved colonic mucosa of AA and NHW CRC cases was compared with normal mucosa of AA and NHW controls. In addition, 16S rDNA sequencing was performed in AA cases and controls. Correlations were examined among bacterial targets, race, disease status and dietary intake.

Results AAs harboured a greater abundance of sulfidogenic bacteria compared with NHWs regardless of disease status. Bilophila wadsworthia-specific dsrA was more abundant in AA cases than controls. Linear discriminant analysis of 16S rRNA gene sequences revealed five sulfidogenic genera that were more abundant in AA cases. Fat and protein intake and daily servings of meat were significantly higher in AAs compared with NHWs, and multiple dietary components correlated with a higher abundance of sulfidogenic bacteria.

Conclusions These results implicate sulfidogenic bacteria as a potential environmental risk factor contributing to CRC development in AAs.

  • COLORECTAL CANCER
  • HYDROGEN SULPHIDE
  • COLONIC MICROFLORA

https://doi.org/10.1136/gutjnl-2016-313321

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    Footnotes

    • CY and PGW share co-first authorship.

    • Contributors Study concept and design (NAE, HRG, PGW and CY); acquisition of data (KV, PGW and CY); analysis and interpretation of data (GJA, NAE, HRG, LTH, EM, T-WL, PGW and CY); drafting manuscript (NAE, HRG, PGW and CY); critical revision of manuscript (NAE, HRG, LTH, BJ, T-WL, XL, PGW, CY and RMX); statistical analysis (GJA, HK and EM); obtained funding (NAE, LTH, BJ, XL, EM and HRG); administrative, technical or material support (CB, TC, XL, LTH, BJ and RMX); study supervision (XL, RMX and HRG).

    • Funding This work was supported by grants from the National Cancer Institute (U01 CA153060 and P30 CA023074, NAE; RO1 CA204808, HRG, EM, LTH; RO1 CA141057, BJ) and the American Cancer Society Illinois Division (223187, XL). PGW was supported by a predoctoral fellowship from Mayo Clinic and University of Illinois Alliance for Technology-Based Healthcare. CY was supported by a training grant from National Institute of Health (5T32DK007788-15). GJA was supported by a Cancer Biology Training Grant (T32CA009213).

    • Competing interests None declared.

    • Ethics approval Institutional review boards of each participating medical centre.

    • Provenance and peer review Not commissioned; externally peer reviewed.