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Antibiotic use and colorectal cancer: a causal association?
  1. Wenjie Ma1,2,
  2. Andrew T Chan1,2,3,4
  1. 1 Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
  2. 2 Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
  3. 3 Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
  4. 4 Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA
  1. Correspondence to Dr Andrew T Chan, Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, MA 02108, USA; achan{at}mgh.harvard.edu

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Antibiotics have revolutionised our ability to fight infectious diseases that are major causes of morbidity and mortality. However, the widespread use of these powerful agents has led to unintended consequences that reflect their broad effects on microbial community structure. Even short-term antibiotic treatment causes shifts in gut microbiota including, but not limited to, alterations in the abundance of specific taxa and a decrease in overall diversity. Clostridium difficile colitis and vaginal candidiasis are established examples of conditions that originate from gut dysbiosis and opportunistic pathogen colonisation induced by short-term antibiotics. Emerging data also suggest that antibiotic-induced perturbations can persist for years after treatment and contribute to long-term dysregulation of host immune homeostasis.1 In turn, this can potentially increase susceptibility to chronic disorders with an immune basis, including asthma, inflammatory bowel disease and obesity.

Recent epidemiological studies have extended the association between antibiotic exposure and chronic disease to risk of colorectal adenoma and colorectal cancer (CRC).2 In parallel, increasing evidence has demonstrated a pivotal role for the interplay between the gut microbiome and lifestyle factors in initiating and promoting CRC.3 Several species of bacteria have been shown to be potential drivers of carcinogenesis through specific biological mechanisms. For example, Fusobacterium nucleatum expresses adhesins, including FadA and Fap2, which bind to tumour cells and directly promote carcinogenesis by activating oncogenic Wnt/β-catenin signalling and dysregulating immune cell infiltration and antitumour immunity. Enterotoxigenic Bacteroides fragilis forms biofilms in the colonic mucosal membrane, …

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Footnotes

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests ATC previously served as a consultant for Janssen Pharmaceuticals, Pfizer Inc and Bayer Pharma AG for work unrelated to the topic.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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